Diagnosis Differential diagnosis Treatment and discharge Instructions

Signs and Symptoms of Thyrotoxicosis - panic attacks, mania, pheochromocytoma, and weight loss associated with malignancy main antithyroid drugs are thionamides: propylthiouracil, carbimazole or methimazole
(Descending Order of Frequency)
Other causes of Thyrotoxicosis CARBIMAZOLE or METHIMAZOLE:
SYMPTOMS: 1. Destructive thyroiditis - (subacute or silent thyroiditis) typically presents with a short thyrotoxic phase due to the 10-20 mg every 8 or 12 hours, OD after euthyroidism is restored.
Hyperactivity, irritability, dysphoria Heat release of preformed thyroid hormones and catabolism of Tg
intolerance and sweating Palpitations 2. thyrotoxicosis factitia, iodine excess, and, rarely, ectopic thyroid tissue, particularly teratomas of the ovary PROPYLTHIOURACIL
Fatigue and weakness Weight loss with (struma ovarii) and functional metastatic follicular carcinoma. 100mg -200 mg every 6-8 hours
increased appetite Diarrhea Polyuria 3. Amiodarone treatment is associated with thyrotoxicosis in up to 10% of patients, particularly in areas of low
Oligomenorrhea, loss of libido iodine intake Thyroid function test and clinical manifestations are reviewed 4-6 weeks after starting treatment.
4. TSH-secreting pituitary adenoma is a rare cause of thyrotoxicosis. It is characterized by the presence of an
SIGNS inappropriately normal or increased TSH level in a patient with hyperthyroidism, diffuse goiter, and elevated T4 TITRATION regimen:
Tachycardia; atrial fibrillation in the elderly and T3 levels 2.5 – 10 mg Carbimazole or Methimazole
Tremor Goiter Warm, moist skin Muscle 50 – 100 mg of Propylthiouracil
weakness, proximal myopathy Lid
retraction or lag Gynecomastia PROPANOLOL: 20 – 40 mg every 6 hours

CLINICAL Manifestations: RADIOIODINE:

- Unexplained weight loss - Carbimazole or methimazole must be xtopped 2-3 days before radioiodine to achieve optimum
- Hyperactivity, nervousness, iodine uotake and can be restarted 3-7 days after redioiodine.
irritability, easy fatigability - RAI dosage 370 mbq – 555 mbq
- Insomnia, impaired - Avoid close or prolohged contact with children and pregnant 5-7 days.
concentration - Persistent hyperthyroidism can be treated with a second dose of radioiodine, usually 6 months after
- Fine tremor the first dose
- Common neurologic - Pregnancy and breast-feeding are absolute contraindications to radioiodine treatment,
manifestation: hyperreflexia, - patients can conceive safely 6 months after treatment
muscle wasting, proximal - presence of ophthalmopathy, especially in smokers, requires caution. Prednisone, 0.2–0.5 mg/kg per
myopathy w/o fasciculation. d (depending on ophthalmopathy severity), at the time of radioiodine treatment, tapered over 6–12
- mc CARDIOVASCULAR SX: weeks
SINUS TACHYCARDIA,
palpitations, SVT, high cardiac Total or near-total thyroidectomy
output -> bounding pulse, - relapse after antithyroid drugs and prefer this treatment to radioiodine
widened pulse pressure and - Careful control of thyrotoxicosis with antithyroid drugs, followed by potassium iodide (SSKI; 1–2
aortic systolic murmur drops orally tid for 10 days to avoid thyrotoxic crisis and to reduce the vascularity of the gland.
- skin: warm and moist, sweating - major complications of surgery—bleeding, laryngeal edema, hypoparathyroidism, and damage to the
and heat intolerance, palmar recurrent laryngeal nerves
erythema, onochylosis, pruritus,
urticaria, diffuse ANTI THYROID DRUGS IN PREGNANCY
hyperpigmentation propylthiouracil should be used until 14–16 weeks
- hair texture fine, diffuse alopecia
- GI: decreased transit time, inc potential for teratogenic effects, recent recommendations suggest discontinuation of antithyroid medication in a
stool frequency, diarrhea, mild newly pregnant woman with Graves’ disease who is euthyroid on a low dose of methimazole (<5–10 mg/d) or
steatorrhea propylthiouracil (<100–200 mg/d)
- women: oligomenorrhea or - propylthiouracil should be limited to the first trimester and then maternal therapy should be
amenorrhea converted to methimazole (or carbimazole) at a ratio of 15–20 mg of propylthiouracil to 1 mg of
- osteopenia, mild hypercalcemia, methimazole.
hypercalciuria
- THYROID: diffusely enlarged
to 2 – 3 x normal size. FIRM not
nodular, +/- thrill or bruit
(inferolateral margins of thyroid
lobes)
- Lid retraction
Graves Disease
- The hyperthyroidism of Graves’
disease is caused by thyroid-
stimulating immunoglobulins
KAMREENA MAGAO- MUSTAFA NOTES
 (TSIs) that are synthesized by
lymphocytes in the thyroid gland
as well as in bone marrow and
lymph nodes

DIAGNOSTICS:
Graves’ disease
- TSH level is suppressed, and
- total and unbound thyroid
hormone levels are increased.
- elevation of bilirubin, liver
enzymes, and ferritin. Microcytic
anemia and thrombocytopenia
-
THYROID STORM GOALS OF MANAGEMENT: THYROID STORM:
- rare and presents as a life-threatening exacerbation of hyperthyroidism, accompanied by fever,
PATHYPHYSIOLOGY 1. Stop synthesis of new thyroid hormones delirium, seizures, coma, vomiting, diarrhea, and jaundice.
- Point at which thyrotoxicosis 2. Halt release of preformed thyroid hormones - precipitated by acute illness (e.g., stroke, infection, trauma, diabetic ketoacidosis), surgery
transforms to storm is 3. Prevent conversion of T4 to T3 (especially on the thyroid), or radioiodine treatment of a patient with partially treated or untreated
controversial 4. Control adrenergic symptoms associated with thyrotoxicosis hyperthyroidism
- No evidence that there is an 5. Control systemic decompensation
increased production of T3 or T4 6. Treat underlying cause MANAGEMENT:
causing the storm - intensive monitoring and supportive care,
- Magnitude of increase in thyroid - identification AND treatment of the precipitating cause, and
hormones does not appear to be - measures that reduce thyroid hormone synthesis.
critical
- Increased catecholamine - Propylthiouracil (500–1000 mg loading dose and 250 mg every 4 h) should be given orally or by
receptors have been noted nasogastric tube or per rectum ) -> iF NOT AVAILABLE
- Decreased binding to thyroid-
stimulating globulin (increased - methimazole can be used in doses of 20 mg every 6 h
free T3/T4) is a possible - One hour after the first dose of propylthiouracil, stable iodide (5 drops SSKI every 6 h)
mechanism - Propranolol should also be given to reduce tachycardia and other adrenergic manifestations (60–80
mg PO every 4 h, or 2 mg IV every 4 h).
- Short-acting IV esmolol can be used to decrease heart rate while monitoring for signs of heart
failure.
- glucocorticoids (e.g., hydrocortisone 300 mg IV bolus, then 100 mg every 8 h)
- antibiotics if infection is present, cholestyramine to sequester thyroid hormones, cooling, oxygen,
and IV fluids.

Ophthalmopathy requires no active treatment when it is mild or moderate,

- Discomfort can be relieved with artificial tears (e.g., hypromellose 0.3% or carbomer 0.2%
ophthalmic gel), paraffin-based eye ointment, and the use of dark glasses with side frames

PERIORBITAL EDEMA:
- Upright sleeping position or diuretic.
Severe ophthalmopathy, with optic nerve involvement or chemosis
- emergency requiring joint management with an ophthalmologist.
- Pulse therapy with IV methylprednisolone (e.g., 500 mg of methylprednisolone once weekly for 6
weeks, then 250 mg once weekly for 6 weeks)
- glucocorticoids are ineffective, orbital decompression can be achieved by removing bone from any
wall of the orbit, thereby allowing displacement of fat and swollen extraocular muscles
Thyroid dermopathy does not usually require treatment,

HYPOTHYROIDISM: COMMON DIAGNOSTICS: MANAGEMENT:

ETIOPATHOGENESIS Sensitive TSH analysis LEVOTHYROXINE

KAMREENA MAGAO- MUSTAFA NOTES
 - Results from undersecretion of - Elevated in primary hypothyroidism
thyroid hormone - May be normal in secondary hypothyroidism (pituitary disease) DOSAGE:
- Iodine deficiency remains the Free T4 - Start usually with 25-50 mcg/day (1.6 mcg/kg/day)
most common cause worldwide - Low in primary hypothyroidism - Use lower dosages of 12.5-25 mcg for patients >60 y/o and those with cardiac disease
- - May be normal in mild hypothyroidism
Duration
Thyroid autoantibodies - Symptoms improve in weeks; lifelong treatment is necessary
Signs and Symptoms of Hypothyroidism - May be noted in autoimmune etiologies - Increase dose by 25-50mcg every 4 weeks until patient is clinically and biochemically euthyroid
(Descending Order of Frequency)
Thyroid scan ultrasound Monitoring
SYMPTOMS - To determine the specific cause of hypothyroidism - Monitor plasma TSH q3-4 months (maintain in normal range)
Tiredness, weakness Dry skin Feeling cold - For secondary hypothyroidism, monitor serum T4 and other pituitary hormones and give steroid
Hair loss Difficulty concentrating and poor replacement prior to LT4
memory Constipation Weight gain with
poor appetite Dyspnea Hoarse voice
Menorrhagia (later oligomenorrhea or
amenorrhea) Paresthesia Impaired hearing

SIGNS
Dry coarse skin; cool peripheral extremities
Puffy face, hands, and feet (myxedema)
Diffuse alopecia Bradycardia Peripheral
edema Delayed tendon reflex relaxation
Carpal tunnel syndrome Serous cavity
effusions

KAMREENA MAGAO- MUSTAFA NOTES

ADRENAL INSUFFICIENCY MANAGEMENT:
- immediate initiation of rehydration, usually carried out by saline infusion at initial rates of 1 L/h
Signs and Symptoms Caused by with continuous cardiac monitoring
Glucocorticoid Deficiency - Glucocorticoid replacement should be initiated by bolus injection of 100 mg hydrocortisone,
- Fatigue, lack of energy Weight followed by the administration of 200 mg hydrocortisone over 24 h, preferably by continuous
loss, anorexia Myalgia, joint pain infusion or alternatively by bolus IV or IM injections.
Fever Normochromic anemia, - Mineralocorticoid replacement can be initiated once the daily hydrocortisone dose has been reduced
lymphocytosis, eosinophilia to <50 mg
Slightly increased TSH (due to Glucocorticoid replacement
loss of feedback inhibition of - oral administration of 15–25 mg hydrocortisone in two to three divided doses
TSH release) Hypoglycemia - dose equivalence: 1 mg hydrocortisone, 1.6 mg cortisone acetate, 0.2 mg prednisolone, 0.25 mg
(more frequent in children) Low prednisone, and 0.025 mg dexamethasone.
blood pressure, postural - Monitoring of glucocorticoid replacement: history and examination for signs and symptoms
hypotension Hyponatremia (due suggestive of glucocorticoid over- or underreplacement, including assessment of body weight and
to loss of feedback inhibition of blood pressure.
AVP release) - All patients with adrenal insufficiency need to be instructed about the requirement for stress-related
glucocorticoid dose adjustments. These generally consist of doubling the routine oral glucocorticoid
Signs and Symptoms Caused by dose in the case of intercurrent illness with fever and bed rest and the need for immediate IV or IM
Mineralocorticoid Deficiency (Primary injection of 100 mg hydrocortisone followed by intravenous infusion of 200 mg hydrocortisone/24 h
Adrenal Insufficiency Only) in cases of prolonged vomiting, surgery, or trauma.
- Abdominal pain, nausea, Mineralocorticoid replacement
vomiting Dizziness, postural - initiated at a dose of 100–150 μg fludrocortisone
hypotension Salt craving Low - monitoring: measuring blood pressure, sitting and standing, to detect a postural drop indicative of
blood pressure, postural hypovolemia.
hypotension Increased serum - serum sodium, potassium, and plasma renin should be measured regularly
creatinine (due to volume - 40 mg of hydrocortisone is equivalent to 100 μg of fludrocortisone.
depletion) Hyponatremia - patients living or traveling in areas with hot or tropical weather conditions, the fludrocortisone dose
Hyperkalemia should be increased by 50–100 μg during the summer
Signs and Symptoms Caused by Adrenal Adrenal androgen replacement
Androgen Deficiency - Adrenal androgen replacement can be achieved by once-daily administration of 25–50 mg DHEA
- Lack of energy Dry and itchy - Treatment is monitored by measurement of DHEAS, androstenedione, testosterone, and sex
skin (in women) Loss of libido hormone–binding globulin (SHBG) 24 h after the last DHEA dose.
(in women) Loss of axillary and
pubic hair (in women)

DIAGNOSIS:
- short cosyntropin test,
- cutoff for failure is usually
defined at cortisol levels of
<450–500 nmol/L (16–18 μg/dL)
sampled 30–60 min after ACTH
stimulation

KAMREENA MAGAO- MUSTAFA NOTES

ETIOPATHOGENESIS The goals of therapy for type 1 or type 2 diabetes mellitus (DM) are to:

- Associated with absolute or (1) eliminate symptoms related to hyperglycemia,

relative insulin deficiency (2) reduce or eliminate the long-term microvascular and macrovascular complications of DM
combined with counterregulatory (3) allow the patient to achieve as normal a lifestyle as possible
hormone excess volume
depletion, and acid base
abnormalities
- Decreased insulin-glucagon ratio
promotes gluconeogenesis,
glycogenolysis and ketogenesis

Manifestations of Diabetic Ketoacidosis

Symptoms: Nausea/vomiting
Thirst/polyuria Abdominal pain Shortness
of breath

Precipitating events: Inadequate insulin

administration Infection (pneumonia/UTI/
gastroenteritis/sepsis) Infarction (cerebral,
coronary, mesenteric, peripheral)
Pancreatitis Drugs (cocaine) Pregnancy

Physical Findings: Tachycardia

Dehydration/hypotension
Tachypnea/Kussmaul respirations/
respiratory distress Abdominal tenderness
(may resemble acute pancreatitis or surgical
abdomen) Lethargy/obtundation/cerebral MANAGEMENT:
edema/possibly coma - Admit to ICU
Diabetes Mellitus: Management and - Measure capillary blood glucose (CBG) every 1-2 hours
Therapies - Monitor BP, pulse, respirations, mental status and fluid I & O every 1-4 hours
Precipitating Factors - Assess serum electrolytes, ABG and renal function
1. Infection: most common FLUID THERAPY:
2. Discontinuation of or inadequate insulin therapy - 15-20 mL/kg/hr or 1-1.5 L of pNSS during the first hour (unless with risk of congestion)
3. Comorbidities such as pancreatitis, MI, stroke - Once CBG is ~200-250 mg/dL, shift fluids to D5-IVF (glucose-containing)
4. Restricted water intake (bedridden, altered thirst response of the elderly) - IVF replacement should correct estimated deficits within the first 34 hours
5. Drugs that affect carbohydrate metabolism: steroids, thiazides, sympathomimetic agents, pentamidine, - in renal/cardiac patients, monitor serum osmolality and cardiac, renal and mental status to avoid
antipsychotics iatrogenic overload
Insulin Therapy
TYPE OF HYPERGLYCEMIC CRISIS: - Regular insulin preferably by IV route (short half-life & easy titration): mainstay of therapy
1. DKA - Initial IV bolus (0.1 unit/kg) is given, then infusion started at 0.1 units/kg/hr (see algorithm)
- Results from increased gluconeogenesis and glycogenolysis and impaired glucose utilization by peripheral - If CBG does not decrease ~50-75 mg/dL/hr, increase insulin infusion rate (two to threefold) hourly
tissues until with a steady glucose decline
- Formerly a hallmark of DM type 1 - When CBG ~200 mg/dL in DKA or 300 mg/dL in HHS, may decrease insulin infusion rate to 0.02-
- Ketones (indicator of DKA) should be measured in individuals with T1DM when glucose > 300 mg/dL 0.05 units/kg/hr to maintain CBG 150-200 mg/dL in DKA or 250-300 mg/dL in HHS
2. HHS Potassium
- Greater degree of dehydration and higher endogenous insulin secretion compared with DKA - Despite depletion of total body potassium, mild-moderate hyperkalemia is common
- Primarily seen in individuals in T2DM - Insulin therapy, correction of acidosis & volume expansion decrease serum K+
- Insulin levels inadequate to facilitate glucose utilization by insulin-sensitive tissues but adequate to prevent
lipolysis and ketogenesis
BICARBONATE
- If pH <6.9, start 100 mmol HCO3 in 400 ml sterile water with 20 mEq KCl at 200 ml/h for 2 hrs
until venous pH >7.0
- Repeat every 2 hours until pH reaches >7.0

KAMREENA MAGAO- MUSTAFA NOTES

RHEUMATOID ARTHRITIS DIFFERENTIALS: TREATMENT:
CLINICAL COURSE: Viral polyarthritis – A viral arthritis is typically suspected in a patient who presents with an inflammatory arthritis and
concomitant evidence of a viral syndrome.Viral polyarthritis generally resolves spontaneously. The treatment of RA adheres to the following principles and goals:
ETIOPATHOGENESIS Osteoarthritis — Osteoarthritis (OA) can be confused with RA in the middle-aged or older patient when the small joints of (1)early, aggressive therapy to prevent joint damage and disability;
Chronic inflammatory disease of the hands are involved. However, different patterns of clinical involvement usually permit the correct diagnosis (2)frequent modification of DMARD therapy to achieve treatment goals with utilization of combination therapy
unknown etiology marked by symmetric, where appropriate;
peripheral polyarthritis (3) individualization of DMARD therapy in an attempt to maximize response and minimize side effects;
Most common form of inflammatory (4)minimal use of long-term glucocorticoid therapy;and
polyarthritis which may result in joint (5)achieving, whenever possible,low disease activity or clinical remission.
damage and physical disability
May result in a variety of extraarticular 1. NSAIDS : Formerly viewed as the core of all other RA therapy Now considered as adjunctive
manifestations (e.g., fatigue, subcutaneous therapy
nodules, lung involvement, pericarditis, 2. GLUCOCORTICOIDS: Low-moderate doses for rapid disease control before the onset of fully
peripheral neuropathy, vasculitis, and effective DMARD therapy
hematologic abnormalities) 1- to 2-week burst of glucocorticoids for acute disease flares

KAMREENA MAGAO- MUSTAFA NOTES

 3. DMARDS : methotrexate DMARD of choice.
Joint Involvement: Slow or prevent structural progression of RA
Initially involves small joints of hands and Cornerstone of therapy
feet 4. BIOLOGICALS – Anti TNF Agents, Anakinra, Abatecept, Rituximab, Anti IL 6 agents
Early morning stiffness >1 hour easing 5. Targeted synthetic DMARDs – Jak Inhibitors
with physical activity 6. Physical activity and assistive devices : Dynamicstrengthtraining,community-
Most frequently involved joints: wrists, basedcomprehensivephysical therapy,andphysical-activity coaching(emphasizing achieving 150 min
MCP, PIP (DIP involvement usually a sign of moderate-to-vigorous physical activity per week). Foot orthotics for painful valgus deformity
of coexistent OA) decrease foot pain and may reduce disability and functional limitations
Swan neck deformity: hyperextension of 7. Surgery: total joint arthroplasty, Silicone implants, Arthrodesis and total wrist arthroplasty are
the PIP with flexion of the DIP joint reserved for patients with severe disease who have substantial pain and functional impairment.
Boutonniere deformity: flexion of the PIP Effective combinations include methotrexate, sulfasalazine,andhydroxychloroquine(oral tripletherapy)
with hyperextension of the DIP joint
Z-line deformity: subluxation of the first Flares during pregnancy are generally treated with low doses of prednisone; hydroxychloroquine and
MCP with hyperextension of 1st IP joint sulfasalazine are probably the safest DMARDs to use during pregnancy.
Flexor tendon tenosynovitis: frequent
hallmark of RA

Subcutaneous Nodules
Seen in 30-40%
Usually benign, firm, nontender and
adherent to periosteum, tendons or bursae

Pleuritic/Pericarditis
Most frequent site of cardiac involvement
in RA is the pericardium

Vasculitis Rheumatoid Arthritis: LABORATORY FEATURES

Fever of >38.3oC during the clinical
course should raise suspicion of systemic - Inc ESR or CRP
vasculitis - Detection of serum RF and anti-CCP antibodies (differentiating RA from other polyarticular diseases)
Others - IgM, IgG, and IgA isotypes of RF occur in sera
Weight loss, fever, fatigue, malaise, - Serum IgM RF has been found in 75% of patients with RA
depression, cachexia in the most severe - presence of serum anti-CCP antibodies (positive test for anti-CCP antibodies in the setting of an early
cases inflammatory arthritis is useful for distinguishing RA from other forms of arthritis)
- 30% of patients with RA test positive for antinuclear antibodies (ANAs)
- antineutrophil cytoplasmic antibodies (ANCAs; particularly p-ANCAs)
SYNOVIAL FLUID ANALYSIS:
- Synovial fluid white blood cell (WBC) rangebetween5000and50,000WBC/ μL
- most useful for confirming an inflammatory arthritis
- excluding infection or a crystal-induced arthritis such as gout or pseudogout
JOINT IMAGING:
- XRAY: periarticular osteopenia, soft tissue swelling, symmetric joint space loss, and subchondral erosions, most
frequently in the wrists and hands (MCPs and PIPs) and the feet (MTPs). advanced RA may reveal signs of
severe destruction, including joint subluxation and collapse
- MRI: greatest sensitivity for detecting synovitis and joint effusions, BONE MARROW EDEMA

KAMREENA MAGAO- MUSTAFA NOTES

 - Ultrasound: power color Doppler, can detect more erosions than plain radiography, increased joint vascularity
indicative of inflammation.

ANTIPHOSPHOLIPID ANTIBODY DIAGNOSIS MANAGEMENT

SYNDROME (APAS) Presence of at least 1 clinical + 1 laboratory criterion
Warfarin (INR 2.5-3.5) after the first thrombotic event
ETIOPATHOGENESIS Pregnancy morbidity prevented by combination of heparin with aspirin 80 mg OD
Autoantibody-mediated acquired IV immunoglobulin may be considered
thrombophilia characterized by recurrent
arterial or venous thrombosis and/or
pregnancy morbidity
Classification and nomenclature of
antiphospholipid antibodies o Antibodies
against cardiolipin (aCL) o Antibodies
against B2GPI (anti-B2GPI) o Lupus
anticoagulant (LA)

GOUTY ARTHRITIS Asymptomatic Hyperuricemia - Defined as hyperuricemia in the absence of gouty arthritis and uric nephrolithiasis MANAGEMENT:
Hyperuricemia; defined as serum uric acid >7 mg/dL (416 umol/L) in men and >6 mg/dL (357 umol/L) in women
ETIOPATHOGENESIS Adequate hydration & increase oral fluid intake (at least 8 glasses of water per day)
KAMREENA MAGAO- MUSTAFA NOTES
 Metabolic disease that usually affects Avoid diuretics unless benefits outweigh the risks
middle-aged to elderly men and
postmenopausal women Results from Acute Gouty Arthritis: Hypouricemic Diet
increased body urate pool with Characterized by acute arthritis initially affecting the MTP of the first toe (podagra) followed by recurring episodes of - Low purine diet, avoid red meals, alcoholic drinks (especially beer)
hyperuricemia acute mono- or oligoarthritis - Limit seafood, sweetened fruit juice / fructose-containing food and beverages
Precipitants of gout: dietary excess, MEDICAL MANAGEMENT:
trauma, surgery, excessive ethanol Chronic Tophaceous Gout (CTG):
ingestion, hypouricemic therapy and Occurs in untreated gouty arthritis, characterized by persistent low grade inflammation of joints with sporadic Asymptomatic Hyperuricemia
comorbid illness (e.g., stroke, ACS) flares Joint deformities: due to deposition of massive urate crystals forming visible tophi - Do not routinely treat with urate lowering medications
- Indications for urate lowering therapy: serum uric acid >11-13 mg/dL, presence of tophi, arthropathy
DIAGNOSTICS on radiography, nephrolithiasis, tumor lysis syndrome, CKD 2-3
Synovial Fluid Analysis
Strongly negative birefringent needle-shaped monosodium urate (MSU) crystals both intra- and extracellularly Acute Attacks
Thick chalky paste fluid; WBC 2,000-60,000/uL - NSAIDS, glucocorticoids, ice compress
- Colchicine: unless contraindicated (e.g., renal insufficiency), colchicine 0.5 mg TID may be given,
Joint Imaging then decreased to OD after the acute attack and maintained until uric acid <6 mg/dL and at least 3
Joint swelling early in the disease; soft tissue masses months without gout flare recurrence
Cystic changes with well-defined erosions and overhanging sclerotic margins
Hypouricemic Therapy
Serum Uric Acid - May be low or normal at the time of attacks - Started 1-2 weeks after acute attacks and continued until uric acid is controlled
24h Uric Acid Urine Collection - Treatment goal is to reduce uric acid to <6 mg/dL
>800 mg/24h (over-producers) - Uric acid under-excretion
<600 mg/24h (under-excretors) - treated with uricosuric drugs (probenecid, benzbromarone, sulfinpyrazone)
- Uric acid over-production
- treated with xanthine oxidase inhibitors:
- Allopurinol 100 mg/tab PO OD initial dose (adjust accordingly) o
- Febuxostat 40 mg/tab ½ tab PO OD initial dose (adjust accordingly)
OSTEOARTHRITIS (OA) DIAGNOSTICS MANAGEMENT
- Goal is relief of pain and prevention of disability
ETIOPATHOGENESIS: No blood tests are routinely indicated
- Most common joint disease and Synovial fluid analysis reveals a non-inflammatory pattern Non-Pharmacologic and Adjunctive Management
a leading cause of disability in Joint imaging correlates poorly with presence and severity of pain: Exercise with brief periods of rest for the involved joint
the elderly May be normal in early stages Weight management (weight loss of 5 kg translates to 50% reduction in pain): core treatment for obese and
- Sine qua non is hyaline articular Advanced stages may show joint space narrowing, subchondral sclerosis, osteophytes overweight adults with knee OA
cartilage loss Correction of possible malalignment (knee braces, orthotics)
- Commonly affected joints are the Acupuncture
cervical and lumbosacral spine, Concentrated standardized ginger preparation
hip, knee and first
metatarsophalangeal (MTP) PHARMACOLOGIC TREATMENT:
joints
- In the hands, the distal and PARACETAMOL
proximal interphalangeal joints Maximum dose of 4 g daily
(IPs) and base of the thumb are First-line drug therapy for reduction of mild knee OA pain
often affected o Wrist, elbow and Close monitoring for upper GI adverse effects for doses >2 g per day
ankle are usually spared
- Risk factors include age (most Low-dose NSAIDs or Selective COX-2 Inhibitors
important), obesity, repeated Up to 2 weeks duration
joint use
- Joint pain is activity-related, Topical NSAIDs
starting as episodic and Less systemic side effects compared to oral preparations
progressing continuously with
accompanying brief morning Intra-articular Injections
stiffness (<30 min) that Steroids: should not exceed 3 times per year in the same joint
gradually resolves Hyaluronans: more effective: longer duration of pain control

Glucosamine and chondroitin sulfate

KAMREENA MAGAO- MUSTAFA NOTES

 Opioids (tramadol)
Topical capsaicin
Surgery (arthroscopic debridement and lavage, meniscectomy, arthroplasty
GUILLAIN-BARRÉ SYNDROME LABORATORY FINDINGS: TREATMENT:

Clinical Manifestations: CSF FINDINGS: - treatment should be initiated as soon after diagnosis as possible.
- rapidly evolving areflexic motor - Elevated CSF protein without pleocytosis - ~2 weeks after the first motor symptoms, it is not known whether immunotherapy is still effective
paralysis with or without sensory - CSF is often normal when symptoms have been present for ≤48h - high-dose intravenous immune globulin (IVIg) - five daily infusions for a total dose of 2g/kg
disturbance body weight.
- ascending paralysis (rubbery DIAGNOSIS: - plasmapheresis (PLEX) ~40–50 mL/kg plasma exchange (PE) 4–5 times over 7–10 days
legs) - AIDP : rapidly evolving paralysis with areflexia, absence of fever or other systemic symptoms, and
- tingling dysesthesias in the characteristic antecedent events Prognosis and Recovery
extremities. - 85% of patients with GBS achieve a full functional recovery within several months to a year,
- bulbar weakness with difficulty DIFFERENTIAL DIAGNOSIS: although minor findings on examination
handling secretions and 1. acute myelopathies (especially with prolonged back pain and sphincter disturbances) - mortality rate is <5% in optimal settings
maintaining an airway 2. diphtheria (early oropharyngeal disturbances
- Pain in the neck, shoulder, back, 3. Lyme polyradiculitis and other tick-borne paralyses
or diffusely over the spine 4. porphyria (abdominal pain, seizures, psychosis)
- Fever and constitutional 5. vasculitic neuropathy (check erythrocyte sedimentation rate
symptoms are absent at the onset 6. poliomyelitis and acute flaccid myelitis (wild-type poliovirus, West Nile virus, enterovirus D68, enterovirus A71,
- Deep tendon reflexes attenuate Japanese encephalitis virus, and the wildtype poliovirus)
or disappear within the first few
days of onset
- Bladder dysfunction may occur
in severe cases
- Autonomic involvement: blood
pressure, postural hypotension,
and cardiac dysrhythmias

ANTECEDENT EVENT:
- GBS occur 1–3 weeks after an
acute infectious process
(respiratory or gastrointestinal)
- Campylobacter, HSV, EBV,
Mycoplasma Pneumoniae
MULTIPLE MYELOMA DIAGNOSIS: TREATMENT:
- marrow plasmacytosis (>10%) - PLASMAPHERESIS and RITUXIMAB
- serum and/or urine M component
HIGH RISK MGUS:
Symptomatic Multiple Myeloma - Repeat every 6 months: serum electrophoresis, cbc, creatinine, and calcium.
Clonal bone marrow plasma cells or biopsy-proven bony or extramedullary plasmacytomaa and any one or more of the
following myeloma-defining events: SYMPTOMATIC MM
•Evidence of one or more indicators of end-organ damage that can be attributed to the underlying plasma cell proliferative 1. systemic therapy to control myeloma
disorder, specifically: 2. supportive care to control symptoms of the disease, its complications, and adverse effects of therapy
•Hypercalcemia: serum calcium >0.25 mmol/L (>1 mg/dL) higher than the upper limit of normal or >2.75 mmol/L (>11
mg/dL) •Renal insufficiency: creatinine clearance <40 mL/minb or serum creatinine >177 μmol/L (>2 mg/dL) Therapy of myeloma includes an initial induction regimen followed by consolidation and/or maintenance
•Anemia: hemoglobin value of >20 g/L below the lower limit of normal, or a hemoglobin value <100 g/L therapy.
•Bone lesions: one or more osteolytic lesions on skeletal radiography, CT, or PET-CTc
•Any one or more of the following biomarkers of malignancy: Hypercalcemia generally responds well to bisphosphonates, glucocorticoid therapy, hydration, and natriuresis
•Clonal bone marrow plasma cell percentagea ≥60% and rarely requires calcitonin as well.
•Involved: uninvolved serum free light chain ratiod ≥100 - Biphosphonates (pamidronate 90 mg or zoledronate 4 mg initially once a month for 12–24 months
•>1 focal lesion on MRI studies and later every 2-3 months)

- Serum protein electrophoresis and measurement of serum immunoglobulins and free light chains are useful for
detecting and characterizing M spikes
- 24-h urine specimen is necessary to quantitate Bence Jones protein (immunoglobulin light chain) excretion

KAMREENA MAGAO- MUSTAFA NOTES

 - CBC May reveal anemia
- ESR is elevated
- Serum calcium, urea nitrogen, creatinine and uric acid levels may be elevated.
- Serum alkaline phosphatase is usually normal even with extensive bone involvement because of the absence of
osteoblastic activity
- Chest and bone radiographs may reveal lytic lesions or diffuse osteopenia
- Magnetic resonance imaging (MRI) offers a sensitive means to document extent of bone marrow infiltration and
cord or root compression in patients with pain syndromes.
-
Acute Cholecystitis DIAGNOSIS
- Acute inflammation of the - triad of sudden onset of RUQ tenderness, fever, and leukocytosis 10,000–15,000 cells per microliter with a left
gallbladder wall usually follows shift on differential count
obstruction of the cystic duct by - serum bilirubin is mildly elevated (<85.5 μmol/L [5 mg/dL])
a stone - elevations in serum aminotransferases
- pain of cholecystitis may radiate - Ultrasound will demonstrate calculi - detection of signs of gallbladder inflammation including thickening of the
to the interscapular area, right wall, pericholecystic fluid, and dilatation of the bile duct
scapula, or shoulder - radionuclide (e.g., HIDA) biliary scan - confirmatory if bile duct imaging is seen without visualization of the
- Peritoneal signs of inflammation gallbladder
such as increased pain with
jarring or on deep respiration Mirizzi’s syndrome
- Anorexia and nausea - is a rare complication in which a gallstone becomes impacted in the cystic duct or neck of the gallbladder causing
- Vomiting compression of the CBD, resulting in CBD obstruction and jaundice.
- Jaundice
- Low grade fever
- Ruq tenderness
- enlarged, tense gallbladder is
palpable
- Deep inspiration or cough during
subcostal palpation of the RUQ
usually produces increased pain
and inspiratory arrest (Murphy’s
sign)
- Localized rebound tenderness in
the RUQ
ASTHMA TREATMENT:
- episodic airway obstruction and
airway hyperresponsiveness ASTHMA ATTACKS
usually accompanied by airway - mild to moderate severity: B-agonist every hour.
inflammation - PEFR >60% of predicted will frequently respond to β2-agonists alone. If they fail to respond in 1–2
h, intravenous corticosteroids should be administered.
- Supplemental oxygen is usually administered to correct hypoxemia.
DIAGNOSIS AND EVALUATION - Failure to achieve PEFR >60% or persistent severe tachypnea over 4–6 h should prompt
consideration of admission to the hospital.
- complain of episodes of - Noninvasive positive-pressure ventilation to assist with respiratory exhaustion is sometimes used
wheezing, shortness of breath, to prevent a need for intubation, and helium-oxygen mixtures may be used to decrease the work of
chest tightness, mucus breathing
production, or cough upon - ANTIBIOTICS: If with sign of infection
exposure to triggers - Mech Vent: aim for low Respiratory rate and/or ventilation volumes to decrease peak airway
pressures. “PERMISSIVE HYPERCAPNIA” -- —allowing the Pco2 to rise and, if necessary,
temporarily correcting critical acidosis

VACCINATION:
- Pneumococcal vaccines, influenza and COVID 19 vaccination.

KAMREENA MAGAO- MUSTAFA NOTES

 -

ST-segment myocardial Infacrtion PHYSICAL FINDINGS: PREHOSPITAL CARE:

- anxious and restless Major elements of prehospital care of patients with suspected STEMI:
PATHOPHYSIOLOGY: - Pallor associated with perspiration and coolness of the extremities 1. recognition of symptoms by the patient and prompt seeking of medical attention;
- coronary blood flow decreases - substernal chest pain persisting for >30 min and diaphoresis strongly suggests STEMI. 2. rapid deployment of an emergency medical team capable of performing resuscitative maneuvers,
abruptly after a thrombotic - ANTERIOR INFARCTION: sympathetic nervous system hyperactivity (tachycardia and/or hypertension) including defibrillation;
occlusion of a coronary artery - INFERIOR INFARCTION: parasympathetic hyperactivity (bradycardia and/or hypotension) 3. expeditious transportation of the patient to a hospital facility that is continuously staffed by
previously affected by physicians and nurses skilled in managing arrhythmias and providing advanced cardiac life support;
atherosclerosis. - physical signs of ventricular dysfunction include fourth and third heart sounds, decreased intensity of the first and
heart sound, and paradoxical splitting of the second heart sound 4. expeditious implementation of reperfusion therapy
CLINICAL PRESENTATION: - transient midsystolic or late systolic apical systolic murmur due to dysfunction of the mitral valve apparatus
1. chest pain- heavy, squeezing and GOALS FOR MANAGEMENT (ER)
crushing/stabbing or burning LABORATORY FINDINGS: 1. control of cardiac discomfort,
2. pain involves the central portion 1. ACUTE (few hours – 7days) 2. rapid identification of patients who are candidates for urgent reperfusion therapy,
of the chest and/or the 2. HEALING (7-28 DAYS) 3. triage of lower-risk patients to the appropriate location in the hospital, and
epigastrium 3. HEALED >29 days 4. avoidance of inappropriate discharge of patients with STEMI.
3. accompanied by weakness,
sweating, nausea, vomiting, LABORATORY TESTS of value in confirming the diagnosis may be divided into FOUR groups: transfer from a non-PCI hospital to one that is PCI capable, with a goal of initiating PCI within 120 min of
anxiety, and a sense of 1. ECG first medical contact
impending doom. 2. Serum cardiac biomarkers
4. sudden-onset breathlessness 3. Cardiac imaging PHARMACOLOGIC THERAPY:
5. less common presentations, with 4. Nonspecific indices of tissue necrosis and inflammation 1. ASPIRIN: chewed 160–325-mg tablet,
or without pain, include sudden followed by daily oral administration of aspirin in a dose of 75–162 mg.
loss of consciousness, a 2. HYPOXEMIA: 02 support administered by nasal prong or face mask 2-4 l/min (first 6-12 hours of
confusional state, a sensation of infarction.
profound weakness, the Control of discomfort:
appearance of an arrhythmia, 3. Nitroglycerin – sublingual 3 doses of 0.4 mg with 5 mins intervals.
evidence of peripheral embolism, - nitrates should be avoided in patients who present with low systolic arterial pressure (<90 mmHg)
or merely an unexplained drop in - clinical suspicion of RV infarction (inferior infarction on ECG, elevated jugular venous pressure,
arterial pressure. clear lungs, and hypotension)
- Nitrates should not be administered to patients who have taken a phosphodiesterase-5 inhibitor for
erectile dysfunction within the preceding 24 h

4. MORPHINE: IV 2-4 mg every 5 minutes

- vagotonic effect and may cause bradycardia or advanced degrees of heart block, particularly in
patients with inferior infarction. (tx: Atropine 0.5 mg IV)

5. IV BETA BLOCKERS - control of the pain

- intravenous beta blockers reduce the risks of reinfarction and ventricular fibrillation
- Metoprolol 5 mg every 2-5 minutes, SBP >100 mmhg, PR interval <0.24 s, rales no higher than
10 cm up from the diaphragm.
- Fifteen minutes after the last intravenous dose, an oral regimen is initiated of 50 mg every 6 h for 48
h, followed by 100 mg every 12 h.

KAMREENA MAGAO- MUSTAFA NOTES

 Oral beta blocker therapy should be initiated in the first 24 h for patients who do not have any of the
following:

(1) signs of heart failure,

(2) evidence of a low-output state,
(3) increased risk for cardiogenic shock, or
(4) other relative contraindications to beta blockade (PR interval >0.24 s, second- or third-degree heart block,
active asthma, or reactive airway disease).

GOUT AND OTHER CRYSTAL- TREATMENT:

ASSOCIATED ARTHROPATHIES
DIAGNOSIS: Non-pharmacologic measures
- confirmed by needle aspiration of involved joints or tophaceous deposits - Ice pack application and rest of the involved joint.

PATHOGENESIS: ACUTE FLARE: Mainstay of acute gout care: NSAIDS, COLCHICINE and glucocorticoids
Gout is a hyperuricemic metabolic - needle-shaped MSU crystals present intracellularly and extracellularly
condition, typically manifested by episodic - Compensated polarized light: bright, negative birefringence NSAIDs:
inflammatory arthritis with disabling pain, - Synovial fluid: cloudy, increased numbers of leukocytes (e.g., from 5000–75,000/μL) 1. Indomethacin 25–50 mg tid
among middle-aged to elderly men and - Large amount crystals: thick, pasty, chalky joint fluid or drainage from distended tophus 2. naproxen, 500 mg bid
postmenopausal women. 3. ibuprofen, 800 mg tid
CHRONIC HYPERURICEMIA: 4. celecoxib, 800 mg followed by 400 mg 12 h later, then 400 mg bid
CLINICAL MANIFESTATIONS: - Serum urate levels can be normal or low at the time of an acute flare
- Acute recurrent gout flares Colchicine:
- One joint affected DIAGNOSTICS: - A low-dose regimen (1.2 mg with the first sign of a flare, followed by 0.6 mg in 1 h (subsequent-day
- 70 – 90 % metatarsophalyngeal - Serum creatinine, liver function tests, hemoglobin, white blood cell (WBC) count, hemoglobin A1c , and serum dosing depending on response)
joint of the first toe (podagra) lipids (obtain as baseline to assess possible risk factor and comorbidities. - additional caution is warranted among patients with hepatorenal impairment.
- Tarsal joints, ankles, knees,
finger, wrist and elbow joints. RADIOGRAPHIC FEATURES: Glucocorticoids: IM or Oral
- Gout flares begin at night to 1. PLAIN RADIOGRAPHY: cystic changes, well-defined erosions with sclerotic margins and soft tissue masses - prednisone, 30–50 mg/d as the initial dose and gradually tapered with the resolution of the attack
early morning 2. Musculoskeletal Ultrasound: double contour sign overlying the articular cartilage - anakinra is a useful option when other treatments are contraindicated or have failed.
- Joints: warm, tender and swollen 3. Dual-energy computed Tomography- presence of MSU crystals
subsides spontaneously within 1- URATE-LOWERING THERAPY
2 weeks. DIFFERENTIAL DIAGNOSIS: - initiated in any patient who already has subcutaneous tophi or chronic gouty arthritis or known uric
- Acute septic arthritis acid stones.
TRIGGERS: - Crystal associated arthropathies
- Purine-rich food, alcohol, - Psoriatic arthritis Allopurinol:
diuretic use, initial introduction - first-line urate-lowering drug among gout patients.
of urate-lowering therapy, local - single morning dose, starting at 100 mg daily or less and titrating up (to 800 mg daily)
trauma and medical illness - target serum urate level <5–6mg/dL
(congestive heart failure and - CKD patients: eGFR 30-45 mL/min start at 50 mg daily and titrate up slowly.
respiratory hypoxic conditions).
Febuxostat
- xanthine oxidase inhibitor
- metabolized by glucuronide formation and oxidation in the liver
- not require dose adjustment in moderate to severe chronic kidney disease

Probenecid
- second-line urate-lowering therapies
- Used in patients with good renal function either alone or in combination with xanthine oxidase
inhibitors such as allopurinol
- Start at a dose of 250 mg twice daily and inc gradually as needed up to 3g/d to achieve and maintain
a target serum urate level.
- not effective in patients with serum creatinine levels >177 μmol/L (2 mg/dL)
-

DIAGNOSTICS:

KAMREENA MAGAO- MUSTAFA NOTES

CALCIUM PYROPHOSPHATE
DEPOSITION DISEASE Definitive diagnosis
CLINICAL MANIFESTATIONS - requires demonstration of typical rhomboid or rodlike crystals
- nee is the joint most commonly - eakly positively birefringent or nonbirefringent with polarized light TREATMENT:
affected, followed by the wrist, 1. Anti-inflammatory
while the first Radiographs or ultrasound reveal punctate and/or linear radiodense deposits within fibrocartilaginous joint menisci or 2. Ice pack application with rest
metatarsophalangeal joint articular hyaline cartilage (chondrocalcinosis), the diagnostic likelihood of CPPD disease is further increased. 3. Joint fluid aspiration
(podagra) is rarely affected 4. Glucocorticoid injection
- Other affected joints include the - leukocyte count in synovial fluid in acute CPPD can range from several thousand cells to 100,000 cells/μL, with 5. Oral colchicine
shoulder, ankle, elbow, and hand the mean being ~24,000 cells/μL and the predominant cell being the neutrophil. 6. NSAIDs
- Acute attacks present sometimes 7. Systemic glucocorticoids
with systemic signs such as
fever, chills, and elevated acute-
phase reactants

PRECIPITATING FACTORS:
1. Trauma
2. Medical illness or surgery
(parathyroidectomy)

CHRONIC CPP CRYSTAL

ARTHRITIS
1. polyarticular arthritis resembling
osteoarthritis
characterized by unusually
severe joint damage in atypical
joints for osteoarthritis, such as
metacarpophalangeal, wrist,
elbow, shoulder, or ankle joints.

CALCIUM APATITE DEPOSITION DIAGNOSIS: TREATMENT:

DISEASE - Nonspecific
Radiograph: Intra- and/or periarticular calcifications with or without erosive, destructive, or hypertrophic changes. - Aspiration of effusions and the use of either NSAIDs or oral colchicine for 2 weeks or intra- or
Pathogenesis Synovial Fluid: synovial fluid leukocyte count in apatite arthritis is usually low (<2000/μL); predominance of mononuclear periarticular injection of a depot glucocorticoid appear to shorten the duration and intensity of
- Abnormal accumulation of basic cells. symptoms.
calcium phosphates, largely
carbonate substituted apatite, can DEFINITVE DIAGNOSIS:
occur in areas of tissue damage - identification of crystals from synovial fluid or tissue
(dystrophic calcification), - crystals are very small and can be seen only by electron microscopy
hypercalcemic or - Clumps of crystals mayappear as 1- to 20-μmshiny intra- or extracellular nonbirefringent globules or aggregates
hyperparathyroid states that stain purplish with Wright’s stain and bright red with alizarin red S
(metastatic calcification),
connective tissue diseases
(calcinosis), and other
conditions.
Clinical Manifestations:

Symptoms range from minimal to severe

pain and disability that may lead to joint
replacement surgery

Mc site of apatite deposition:

- bursae and tendons in and/or
around the knees, shoulders,
hips, and fingers

KAMREENA MAGAO- MUSTAFA NOTES

 Apatite aggregates are often present in
synovial fluid in an extremely destructive
chronic arthropathy of the elderly that
occurs most often in the shoulders
(Milwaukee shoulder) and in a similar
process in hips, knees, and erosive
osteoarthritis of fingers.
CAOX DEPOSITION DISEASE: Clinical manifestions and Diagnosis TREATMENT:

Pathogenesis: - Clinical features of acute CaOxarthritismaynotbedistinguishablefrom those due to MSU, CPP, or apatite. - NSAIDs, Colchicine, Intraarticular glucocorticoids, and/or an increased frequency of dialysis has
- Ascorbic acid is metabolized to - Deposits have been documented in fingers, wrists, elbows, knees, ankles, and feet. prodcued slight improvement.
oxalate, which is inadequately
cleared in uremia and by Radiographs Primary oxalosis:
dialysis. Such supplements and - reveal chondrocalcinosis or soft tissue calcifications. Liver transplantation – significant reduction in crystal deposits.
foods high in oxalate content
usually are avoided in dialysis CaOx-induced synovial effusions
programs because of the risk of - noninflammatory, with <2000 leukocytes/μL, or mildly inflammatory.
enhancing hyperoxalosis and its - Neutrophils or mononuclear cells can predominate
sequelae. - CaOx crystals have a variable shape and variable birefringence to polarized light.
- most easily recognized forms are bipyramidal, have strong birefringence, and stain with alizarin red S.
ACUTE RHEUMATIC FEVER TREATMENT:

Clinical features: 1. Antibiotics:

- latent period of ~3 weeks (1– - Penicillin is the drug of choice and can be given orally 500 mg BID PO
5weeks)betweentheprecipitating - Amoxicillin 50 mg/kg daily (max 1 gram) x 10 days
group A streptococcal infection - Benzathine Penicillin G single dose of 1.2 million units IM
and the appearance of the
clinical features of ARF 2. Salicylates and Nsaids
- most common clinical features 3. Glucocorticoids (CHF)
are polyarthritis (present in 60– 4. Management of Heart Failure (bed rest)
75% of cases) and carditis (50– 5. Chorea (Carbamazepine or sodium valproate), IVIG
75%), chorea (<2-3%), erythema
marginatum and subcutaneous
nodules are rare (<5%)

HEART INVOLVEMENT
- Valvular damage is the hallmark
of rheumatic carditis.
- mitral valve is almost always
affected

1
KAMREENA MAGAO- MUSTAFA NOTES