PCM Spring Exam Material
I.
Anemia
a. General Approaches to Anemia- Hematocrit < 41% in males, <37% in females
b. Iron Deficiency Anemia
i. Essentials of Diagnosis:
1. Both pathognomonic; absent bone marrow iron stores or serum
ferritin < 12ug/L
2. Caused by bleeding in adults unless proved otherwise
3. Response to iron therapy
ii. General Considerations: Causes- Deficient iron, decreased absorption,
increased requirements (Pregnancy, lactation), blood loss (GI, menstrual,
donation), hemoglobinuria, iron sequestration (pulmonary hemosiderosis)
iii. Clinical Findings
1. S/S:
a. Easily fatigability, tachycardia, palpitations and tachypnea
on exertion
b. Severe deficiency: Skin and mucosal changes (smooth
tongue, brittle nails, and cheilosis)
c. Dysphagia: formation of esophageal webs (PlummerVinson syndrome)
d. Pica: craving for specific foods- ice chips, lettuce, etc
2. Labs:
a. Hypochromic microcytic cells on smear
b. Low serum ferritin <30ug/L
c. Increase in total iron binding capacity
iv. Differential Diagnosis
1. Anemia of chronic disease: Normal or ↑ iron stores, normal or ↑
ferritin levels, serum iron is low, TIBC is low or normal
2. Thalassemia: Family hx., microcytosis
3. Sideroblastic anemia
v. Treatment
1. Iron replacement: Oral or parenteral iron
2. ID cause
c. Anemia of Chronic Disease
i. Clinical Findings:
1. Patient with known chronic disease
2. Low serum iron, low TIBC, and normal or increased serum ferritin
3. If severe: Suspect co-existing Fe deficiency or folic acid deficiency
4. Labs: Normal MCV, Normal blood smear
ii. Treatment:
1. Usually none
2. Combinant erythropoietin
d. Vitamin B12 Deficiency
i. Essentials of Diagnosis:
1. Macrocytic anemia
2. Macro-ovalocytes and hypersegmented PMN on peripheral smear
3. Serum vit B12 levels < 100pg/mL
ii. General Considerations: Causes- Dietary deficiency (RARE-see only in
vegans), Decreased production of IF (pernicious anemia, gastrectomy), H.
pylori infection, competition for vit. B12 in gut (Blind loop syndrome, fish
tapeworm-rare), Pancreatic insufficiency, Decreased ileal absorption of
vit. B12 (Surgical resection, Crohn’s), Transcobalamin II deficiency (rare)
iii. Clinical Findings:
1. S/S:
a. Glossitis, anorexia, diarrhea,
b. Complex neurological syndrome (peripheral neuropathy,
impairment of posterior columns, difficulty with balance),
dementia, decreased vibration and position sense
c. Pale, mildly icteric
2. Labs: Megaloblastic anemia, hematocrits as low as 10-15%
iv. DDx: Folic acid deficiency, myelodysplasia, nonhematologic pernicious
anemia
v. Treatment: Parenteral therapy- IM injection of vit. B12; oral cobalamin
e. Folic Acid Deficiency
i. Essentials of Diagnosis:
1. Macrocytic anemia
2. Macro-ovalocytes and hypersegmental PMN on peripheral smear
3. Normal serum vit. B12 levels
4. Reduced folate levels in RBC of serum
ii. General Considerations: Causes- Dietary deficiency, decreased absorption
(Tropical sprue, drugs), increased requirement (chronic hemolytic anemia,
pregnancy, exfoliative skin disease), loss (dialysis), inhibition of reduction
to active form (MTX)
iii. Clinical Findings
1. Similar to vit. B12- NO neurological changes
2. Megaloblastic anemia
3. Megaloblastic changes in mucosa
iv. DDx: Vit. B12 deficiency, Alcoholic (anemia of liver disease),
hypothyroidism
v. Treatment: Folic acid
f. Hemolytic Anemia
g. Sickle Cell Anemia and related syndromes
i. Essentials of diagnosis:
1. Irreversibly sickled cells on peripheral blood smear
2. Positive family history and lifelong history of hemolytic anemia
3. Recurrent painful episodes
4. Hemoglobin S is the major hemoglobin seen on electrophoresis
ii. Clinical Findings:
1. Chronic hemolytic anemia: jaundice, pigment gallstones,
splenomegaly-initially, and poorly healing ulcers over lower tibia
2.
3.
4.
5.
II.
III.
Enlarged heart: hyperdynamic precordium and systolic murmurs
Hemolytic crisis- splenic sequestration
Aplastic crisis
Vaso-occlusive crisis: acute painful episodes with low-grade fever,
provoked by infection, dehydration, or hypoxia; last hours to days
6. Prone to delayed puberty
7. Prone to infections: hyposplenism
iii. Labs: Peripheral blood smear, CBC, hematocrit, Sickledex
iv. Treatment: Folic acid supplements, transfusion for crisis, treat
precipitating conditions, kept well hydrated and oxygenated; Hydroxyurea
for vaso-occlusive crisises
h. Aplastic Anemia
i. Essentials of Diagnosis
1. Pancytopenia
2. No abnormal cells seen
3. Hypocellular bone marrow
ii. Genral Considerations: Causes- Congenital (rare), Idiopathic, SLE,
Chemo, radiation, Toxins (benzene, toluene, insecticides), drugs,
posthepatitis, pregnancy, paroxysmal nocturnal hemoglobinuria
iii. Clinical Findings:
1. S/S:
a. Bone marrow failure  weakness, fatigue, neutropenia
(bacterial infections), thrombocytopenia (mucosal and skin
bleeds)
b. PE: Pallor, purpura, petechiae
c. NOT present: Hepatosplenomegaly, lymphadenopathy, or
bone tenderness
2. Labs: CBC, blood smear, bone marrow aspirate
iv. DDx: Myelodysplatic disorders or acute leukemia
v. Treatment: Supportive care, RBC and platelet transfusion, antibiotics for
infections, BMT, If BMT is not possible: immunosuppression with
antithymocyte globulin plus cyclosporine
Geriatric SKIP
Kidney Disease
a. Glomerulonephritis 872-873
i. Essentials of Diagnosis
1. Hematuria, dysmorphic red cells, red cell casts, and mild
proteinuria
2. Dependent edema and hypertension
3. Acute renal insufficiency
ii. General Considerations: Uncommon cause of acute renal failure
iii. Clinical Findings
1. HTN, edema (first peri-orbital and scrotal), abnormal sediment
2. Labs: Hematuria, moderate proteinuria, cellular elements
iv. Treatment: Depends on severity: high dose CST and cytotoxic agests;
plasma exchange for Goodpasture’s
IV.
b. Nephritic Syndrome
i. Essentials of Diagnosis
1. Edema
2. HTN
3. Hematuria (w/ or w/o dysmorphic red cells, red cell casts)
ii. General Considerations: Rapidly progressive acute GN can cause
permanent damage to glomeruli
iii. Clinical Findings:
1. S/S: Edema (first peri-orbital and scrotal), HTN (due to volume
overload)
2. Labs: Serum: Complement levels, ANA, cryoglobulins, hepatitis
panels, ANCA, anti-GBM ab, ASO titers, and C3 nephritic factors;
Urinalysis; Biopsy
iv. Treatment: Reduce HTN and fluid overload; therapeutic management of
underlying cause; Salt and water restriction, diuretic therapy, dialysis if
needed; may require CST and cytotoxic agents
Hypertension
a. Management of Hypertension
i. Etiologies and Classifications
1. Primary (85%): Onset between 25-55 yo; early in course BP
fluctuates
a. Classification:
i. Optimal: <120/<80
ii. Normal: <130/<85
iii. High-normal: 130-139/85-90
iv. HTN Stage 1: 140-159/90-99
v. HTN Stage 2: 160-179/100-109
vi. HTN Stage 3: >180/>110
b. Factors involved in pathogenesis: genetics, hyperactive
sympathetic NS, renin-angiotension system, defect in
natriuresis, intracellular Na and Ca (both increased)
c. Risk factors: obesity, sodium intake, alcohol, smoking,
exercise, polycythemia, NSAID (increase), potassium
intake (low intake associated with higher BP)
2. Secondary
a. Estrogen use
b. Renal Disease
c. Renal vascular HTN
d. Primary hyperaldosteronism and Cushing’s
e. Pheochromocytoma
f. Coarctation of the aorta
g. HTN associated with pregnancy
ii. Complications of untreated HTN (due to sustained elevated BP  changes
in vasculature and heart)
1. HTN cardiovascular disease
2. HTN cerebrovascular disease and dementia (stroke)
V.
3. HTN renal disease
4. Aortic dissection
5. Atherosclerotic complication
iii. Clinical Findings: Asymptomatic
1. HA: suboccipital pulsating HA that are worse in the morning
2. Accelerated HTN: somnolence, confusion, visual disturbances,
nausea and vomiting
3. Pheochromocytoma: Sustained HTN or episodic HTN; attacks of
anxiety, palpitations, profuse perspiration, pallor, tremor, nausea
and vomiting; markedly elevated BP; angina and acute pulmonary
edema may occur
4. Primary aldosteronism: Muscular weakness, polyuria, and nocturia
due to hypokalemia; malignant HTN is RARE; chronic HTN 
ventricular hypertrophy; exertional and paroxysmal nocturnal
dyspnea
5. Cerebral involvement: Stroke due to thrombosis or small or large
hemorrhage from microaneurysms; HTN encephalopathy
6. Signs:
a. BP – take in both arms and lower extremities if pulse is
absent, orthostatic
b. Retinas: Narrowing of arterial diameter, exudates,
hemorrhages, or papilledema
c. Heart and arteries: Systolic ejection murmurs from
calcified aortic sclerosis
d. Pulses: Compare upper and lower extremities
iv. Nonpharmacologic Therapy
1. DASH diet, weight reduction, reduce alcohol, reduce salt, gradual
increase in exercise, smoking cessation
v. Who should be treated with medication
1. Patients in stage II or III
2. Patients that are high normal or stage I are treated with drugs if
they have certain risk factors
vi. Goals of Treatment: Reduce cardiovascular risk and further complications
vii. Drug Therapy
1. Diuretic
2. β-adrenergic blocking agents
3. ACE inhibitors
4. ARB’s
5. Calcium channel blockers
6. α-adrenergic receptor blockers
7. Drugs with central sympatholytic action
8. Arteriolar dilators
9. Peripheral sympathetic inhibitors
Hyponatremia and Hypernatremia
a. Approach to the Patient:
i. Volume overload: Increased weight, peripheral edema, ascites
ii. Volume depletion: Weight loss, excessive thirst, dry mucous membranes
iii. Dehydration: Pure water deficit
b. Hyponatremia
i. Essentials of Diagnosis
1. Extracellular fluid and serum osmolality are important
determinants of etiology
2. Most cases result from water imbalance, not sodium imbalance
ii. Urine sodium:
1. If > 20 meq/L: Renal salt wasting
2. If < 10meq/L: Avid sodium retention due to extrarenal Sodium
wasting
iii. Isotonic Hyponatremia: Hyperlipidemia and hyperproteinemia 
displaces water  Decreased sodium conc. In total plasma volume
iv. Hypertonic Hyponatremia: Seen with hyperglycemia, water drawn from
cells into extracellular space when blood glucose is high. Increase in
glucose causes drop in sodium.
v. Hypotonic Hyponatremia: Retention of electrolyte-free water due to
impaired excretion
1. Hypovolemic hypotonic hyponatremia: Renal or extrarenal volume
loss ADH excretion  Free water retention
2. Euvolemic Hypotonic Hyponatremia:
a. SIADH
b. Hypothyroidism- not common; water retention
c. Psychogenic polydispia and beer potomania: Marked
excess of free water intake
d. Idiosyncratic diuretic reaction: Euvolemic patients on
diuretics  xs renal sodium loss and water retention
e. Idiosyncratic ACE inhibitor reactions: Central polydipsia
and increased ADH secretion
f. Endurance exercise hyponatrium: Xs fluid overload and
continued ADH secretion
g. Mineralcorticoid-responsive hyponatremia in elderly
vi. Treatment
1. Treat underlying cause and Water restriction
2. Diuretics
3. Hypertonic saline: NOT usually recommended
vii. Hyponatremia in AIDS: Associated with pneumonia and CNS processes;
euvolemic SIADH
c. Hypernatremia
i. Essentials of Diagnosis
1. Occurs most commonly when water intake or water
supplementation is inadequate
2. Urine osmolality helps differentiate renal from nonrenal water loss
ii. Clinical Findings
1. S/S: Orthostatic hypotension, oliguria are common. Hyperthermia,
delirium, and coma with severe hyperosmolality
VI.
VII.
2. Labs:
a. Urine osmolality > 400 mosm/kg – renal water-conserving
ability is functioning: Renal vs. non-renal losses
b. Urine osmolality < 250 mosm/kg – Dilute urine with
hypernatremia is characteristic of central and nephrogenic
diabetes insipidus
iii. Treatment:
1. With hypovolemia: Isotonic saline
2. With Euvolemia: Drink water, 5% dextrose and water IV
3. With hypervolemia: 5% dextrose in water + loop diuretic
Renal Calculi
a. Urinary Stone Disease
i. Clinical Finding: Colic pain, localized to flank, associated with nausea and
vomiting (in constant motion), radiate anteriorly over abdomen; if lodged
at ureterovesical junction causes urinary urgency and frequency.
ii. Labs: Serum calcium, phosphate, electrolytes, and uric acid. Urinalysis,
plain film and renal U/S, spiral CT
iii. Medical Treatment and Prevention
1. Increased fluid intake
2. Sleep stone side down
iv. Surgical treatment: Ureteroscopic stone extraction; shock wave lithotripsy
– external energy source fragment stone and lets it pass (not good for
women of childbearing age)
Benign Prostatic Hyperplasia
a. Essentials of Diagnosis:
i. Obstruction or irritative voiding symptoms
ii. May have enlarged prostate on rectal examination
iii. Absence of urinary tract infection, neurologic disorders, stricture disease,
prostatic or bladder malignancy
b. General Consideration: Older men, genetics (?), DHT sensitivity
c. Clinical Findings:
i. Obstructive: hesitancy, decreased force and caliber of the stream,
sensation of incomplete bladder emptying, double voiding, straining to
urinate, and postvoid dribble
ii. Irritative: Urgency, frequency, and nocturia
iii. Questions to ask:
1. Over last month, how often have you had the sensation of not
completely emptying your bladder after finishing urination?
2. How often have you had to urinate again less than 2 hrs after you
finish urinating?
3. How often have you found you stopped and started again several
times when you urinated?
4. How often have you found it difficult to postpone urination?
5. How often have you had a weak urine stream?
6. How often have you had to push or strain to begin urination?
VIII.
7. How many times did you most typically get up to urinate from the
time you went to bed at night until the time you got up in the
morning?
iv. Signs: PE, DRE, and focused neurological exam on all patients, lower
abdomen examination (assess fullness of bladder)
v. Labs: PSA, urinalysis, electrolyte panel
d. DDx: Prostatic carcinoma, renal insufficiency, UTI, urethral stricture, bladder
stone
e. Treatment: Mild symptoms: Watchful waiting; Absolute surgical indications are
refractory urinary retention; MEDS: α-blocker, 5α-Reductase inhibitors,
combination therapy, phytotherapy; Surgery: TURP
Menopause
a. Menopausal Syndrome
i. Essentials of Diagnosis:
1. Cessation of menses due to aging or to bilateral oophorectomy
2. Elevation of FSH and LH levels
3. Hot flushes and night sweats
4. Decreased vaginal lubrication; thinned vaginal mucosa with or
without dyspareunia
ii. Clinical Findings:
1. Menstrual cycles become irregular and longer, menopause occurs
when menstruation has not occurred for one year;
2. Hot flushes; vaginal atrophy (decreased introitus, vaginal dryness,
pale, smooth vaginal mucosa, small cervix and uterus);
osteoporosis
3. Labs: Elevated serum FSH and LH; Vaginal cytology: Parabasal
cell (loss of maturation due to hypoestrinism)
iii. Treatment: Education; vasomotor symptoms: HRT (mention risks);
vaginal atrophy: HRT, estradiol vaginal ring, short-term use of estrogen
vaginal cream; Osteoporosis: Calcium fortified foods (1000mg per day +
vit D)
b. Primary Amenorrhea- >14 yo, no breast development, height in lowest 3%; or
greater than 16 with no menstruation
i. Etiology:
1. Hypothalamic-pituitary causes: Low-normal FSH
2. Hyperandrogenism: Low-normal FSH
3. Ovarian causes: High FSH; Turners, AI
4. Pseudohermaphroditism: High LH
5. Uterine Causes: Normal FSH
6. Pregnancy: High hCG
ii. Clinical Findings: Hx. and PE
1. HA or visual field abnormalities implicate a hypothalamic or
pituitary tumor;
2. Signs of pregnancy;
3. BP abnormalities, acne, and hirsutism should be noted;
IX.
4. Short stature with gonadal dysgenesis indicates Turner’s
syndrome;
5. Olfaction testing for Kallmann’s syndrome;
6. Obesity and short stature may be a sign of Cushing’s;
7. Tall stature may be due to eunuchoidism or gigantism;
8. Hirsutism or virilization suggest excessive testosterone;
9. external pelvic exam – assess hymenal patency and presence of
uterus
10. LABS: Serum FSH, LH, PRL, testosterone, TSH, free T4, and
hCG
iii. Treatment: Directed at the underlying cause
c. Secondary Amenorrhea and Menopause
i. Etiology:
1. Pregnancy: High hCG
2. Hypothalamic-Pituitary Cause: Low-normal FSH
3. Hyperandrogenism: Low-normal FSH
4. Uterine Causes: Normal FSH
5. Premature Ovarian Failure: High FSH
6. Menopause: High FSH
ii. Clinical Findings: Hx and PE
1. Nausea and breast engorgement: pregnancy
2. Hot flushes: Ovarian failure
3. HA or visual field abnormalities: Pituitary or hypothalamic tumor
4. Thirst, polyuria: diabetes insipidus  hypothalamic lesion
5. Goiter: Hyperthyroidism
6. Weight loss, diarrhea, or skin darkening: Adrenal insufficiency
7. Weight loss and distorted body image: Anorexia
8. Galactorrhea: hyperprolactenemia
9. Hirsutism or virilization suggest excessive testosterone
10. Hypercortisolism: Alcohol or Cushings
11. Acromegaly, gigantism: pituitary tumor
12. Systemic illness, drugs
13. Pelvic exam: uterine and adnexal enlargement, PAP, vaginal smear
14. LABS: Serum hCG, testosterone, PRL, FSH, LH, TSH, plasma K;
renal and liver panel
iii. Treatment: Directed at cause. HRT can relieve symptoms. If labs are
normal and not pregnant: 10d course of progestin
Diabetes
a. Essentials of Diagnosis:
TYPE 1 DIABETES
i. Polyuria, polydispia, and weight loss associated with random plasma
glucose > 200 mg/dl
ii. Plasma glucose of 126 mg/dl or higher after an overnight fast, documented
on more than one occasion
iii. Ketonemia, ketonuria, or both
TYPE 2 DIABETES
i. Most patients are over 40 yo and obese
ii. Polyuria and polydipsia. Ketonuria and weight loss generally are
uncommon at time of diagnosis. Candidal vaginitis in women may be an
initial manifestation. Many patients have few or no symptoms
iii. Plasma glucose of 126 mg/dl or higher after an overnight fast on more
than one occasion. After 75 g oral glucose, diagnostic values are 200
mg/dl or more 2 hrs after oral glucose.
iv. HTN, dyslipidemia, and atherosclerosis are often associated
b. Clinical Findings:
Polyuria and thirst
Weakness or fatigue
Polyphagia with weight loss
Recurrent blurred vision
Vulvovaginitis or pruritus
Peripheral neuropathy
Nocturnal enuresis
Often asymptomatic
X.
Type 1 Diabetes
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Type 2 Diabetes
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c. Labs:
i. Urinalysis: Glucosuria, ketonuria
ii. Blood testing procedures: Glucose tolerance test, glycated hgb, serum
fructosamine, self-monitoring of blood glucose, continuous glucose
monitoring system, lipoprotein abnormalities in diabetes
d. DDx.: Hyperglycemia secondary to other causes (Cushing’s, CST, acromengaly,
liver disease, muscle disorders…); Non-diabetic glycosuria
e. Goals of Treatment: Pt. ed, restore known metabolic derangements toward normal
in order to prevent and delay progression of diabetic complications
f. Treatment: Pt. ed, diet, oral agents, insulin
Diseases of the Thyroid
a. Tests of Thyroid Function: TSH (most sensitive), free T4; thyroid radioactive
iodine uptake and scan
b. Hypothyroidism and Myxedema
i. Essentials of Diagnosis
1. Weakness, fatigue, cold intolerance, constipation, weight change,
depression, menorrhagia, hoarseness
2. Dry skin, bradycardia, delayed return of deep tendon reflexes
3. Anemia, hyponatremia
4. T4 and radioiodine uptake usually low
5. TSH elevated in primary hypothyroidism
ii. Clinical Findings:
1. Early: Fatigue, lethargy, weakness, arthralgias or myalgias, muscle
cramps, cold intolerance, constipation, dry skin, HA, and
menorrhagia PE: Thin, brittle nails, thinning of hair, and pallor,
poor mucosa turgor, decreased return of deep tendon reflexes
2. Late: Slow speech, absence of sweating, constipation, peripheral
edema, pallor, hoarseness, decreased sense of taste and smell,
muscle cramps, aches and pains, dyspnea, weight changes,
diminished auditory acuity PE: goiter, puffiness of face,
XI.
carotenemic skin color, thinning of outer eyebrows, thickening of
tongue, hard pitting edema, effusions
3. Labs: Free T4: normal to low; TSH: increased in primary, low or
normal in pituitary insufficiency; Lipid panel (increased
cholesterol), increased liver enzymes, CK…
iii. DDx: Unexplained heart failure, primary amyloidosis, pernicious anemia,
depression
iv. Complications: Mostly cardiac (advanced CAD), megacolon, increased
susceptibility to infection, organic psychoses, rarely causes infertility,
miscarriage, can progress to myxedema coma
v. Treatment: Thyroid replacement therapy, usually T4; reassess T4 levels
regularly
c. Hyperthyrodism
i. Essentials of Diagnosis
1. Sweating, weight loss or gain, anxiety, loose stools, heat
intolerance, irritability, fatigue, weakness, menstrual irregularities
2. Tachycardia; warm, moist skin; stare; tremor
3. In Grave’s disease: goiter, ophthalmopathy
4. Suppressed TSH in primary hyperthyroidism; increased T4, free
T4 and free T4 index
ii. General Considerations: Grave’s disease, Toxic adenomas, subacute
thyroiditis, jodbasedow disease (iodine-induced hyperthyroidism),
thyrotoxicosis factitia, struma ovarii, pituitary tumor, hashimoto’s
thyroiditis, pregnancy and trophoblastic tumors, thyroid carcinoma,
amiodarone-induced thyrotoxicosis
iii. Clinical Findings: SEE Essentials of Diagnosis; LABS: T4 an TSH levels,
serum TSH receptor antibody, serum ANA and anti-dsDNA,
sedimentation rate, thyroid radioactive iodine uptake and scan
iv. DDx: Anxiety, mania, acute psychiatric disorder, cardiac disease,
hypermetabolism (pheochromocytoma), diabetes, Addison’s
v. Complications: Cardiac complication, periodic paralysis w/ exercise or
heavy carb intake, hypercalcemia, osteoporosis, and nephrocalcinosis
vi. Treatment: Depends on cause
1. Graves: Propanol for sympathetic relief, thiouria drug,
methimazole, propylthiouracil, iodinated contrast agents,
radioactive iodine (destroys active thyroid tissue)- not to pregnant
women
Metabolic Bone Disease
a. Osteoporosis
i. Essentials of Diagnosis
1. Asymptomatic to severe backache from vertebral fractures
2. Spontaneous fractures often discovered incidentally on
radiography; loss of height
3. Serum parathyroid hormone, 25(OH)D2, Ca, phosphorous, and
alkaline phosphatase usually normal
4. Demineralization, esp. of spine, hip, and plevis
XII.
ii. Etiology
1. Hormonal deficiency: Estrogen, androgen
2. Hormonal Excess: Glucocorticoid, thyrotoxicosis,
hyperparathyroidism
3. Immobilization, microgravity
4. Tobacco, Alcoholism
5. Malignancy, esp multiple myeloma
6. Meds: xs. Vit D, xs. Vit A, heparin therapy
7. Genetic: Aromatase deficiency, Type I collagen mutations,
Osteogenesis imperfecta, idiopathic juvenile and adult
osteoporosis, Ehlers-Danlos syndrome, Marfan’s syndrome,
homocystinuria
8. Misc: Anorexia, protein-calorie malnutrition, vit. C deficiency,
copper deficiency, liver disease, RA, uncontrolled DM, systemic
mastocytosis
iii. Clinical Findings: Usually asymptomatic until fracture occurs; backache;
loss of height; LABS: Serum Ca, phosphate and PTH are normal, test for
thyrotoxicosis, hypogonadism, and vit. D deficiency; DEXA scan
iv. DDx.: See possible etiologies
v. Treatment: Sex hormones, biphosphonates (inhibit osteoclast-induced
bone resorption), selective estrogen receptor modulators (SERMs),
calcitonin, calcium and vit. D, teriparatide (analog of PTH)
vi. Prognosis: Good if interventions are started early
b. Osteomalacia
i. Essentials of Diagnosis
1. Painful proximal muscle weakness; bone pain and tenderness
2. Decreased bone density from diminished mineralization of osteoid
3. Lab abnormalities may include increases in alkaline phosphatase,
decreased 25-hydroxy-vitamin D, or hypocalciumia, hypocalciuria,
hypophosphatemia, secondary hyperparathyroidism
4. Classic radiologic features may be present
ii. General Considerations:Commonly caused by a deficiency in vit. D
iii. Etiology: Vit. D deficiency and resistance, deficient calcium intake,
phosphate deficiency, aluminum toxicity, hypophosphatasia, fibrogenesis
imperfecta ossium
iv. Clinical Findings: Depends on age and severity; ADULTS: asymptomatic
at first followed by bone pain and muscle weakness, fractures may occur;
CHILD: Ricketes
v. Diagnostic Tests: LABS: Serum calcium, albumin, phosphate, alkaline
phosphatase, PTH, and 25-hydroxyvitamin D; DEXA
vi. DDx.: Osteoporosis (fairly neg. labs)
vii. Prevention and Treatment: Treat underlying cause; sunlight exposure and
vit. D supplements, oral calcium
Arthridities
a. Diagnosis and evaluation
i. Examination of the patient: Presence or absence of extra-articular
manifestations: Is inflammation present? How many joints are involved?
And What joints are affected?
1. Joint inflammation is manifested by redness, warmth, swelling,
and morning stiffness of at least 30 min
b. Degenerative Joint Disease
i. Essentials of diagnosis
1. Commonly secondary to other articular disease
2. A degenerative disorder without systemic manifestations
3. Pain relieved by rest; morning stiffness brief; articular
inflammation minimal
ii. General considerations: PRIMARY: Commonly affects some or all of the
following: terminal interphalangeal joints, proximal interphalangeal joints,
the metacarpophalangeal and carpometacarpal joints of the thumb, the hip,
the knee, the metatarsophalangeal joint of the big toe, the cervical and
lumber spine SECONDARY: Occurs in any joint as a sequela to articular
injury (acute or chronic, metabolic or neurologic disease)
iii. Clinical findings S/S: Insidious onset; Initial: Articular stiffness < 15 min
 Pain on motion of the affected joint  deformity, crepitus; joint
effusion and inflammation are mild; LABS: none; IMAGE: Radiographs,
joint aspiration
iv. DDx.: Usually not confused with other forms of arthritis
v. Prevention: Weight loss, HRT, maintaining normal vit. D level
vi. Treatment: Weight loss, NSAIDS, surgical measures if all else fails and is
debilitating
vii. Prognosis: Better than RA, can be severe and debilitating
c. Crystal Deposition Arthritis (Gouty arthritis)
i. Essentials of diagnosis
1. Acute onset, typically nocturnal and usually monoarticular, often
involving the 1st metatarsopharyngeal joint
2. Postinflammatory desquamation and pruritus
3. Hyperuricemia in most, ID of urate crystals in joint fluid or tophi is
diagnostic
4. Dramatic therapeutic response to NSAIDs or colchicine
5. With chronicity, urate deposits in subcutaneous tissue, bone,
cartilage, joints, and other tissue
ii. General considerations: Primary vs. secondary
iii. Clinical findings:
1. S/S: Sudden onset, frequently nocturnal, w/ or w/o obvious
precipitation due to fluctuating serum urate levels; intense pain as
the attack progresses; affected joint is swollen, tender; overlying
skin is tense, warm, and dusky red; local desquamation and
pruritis; tophi found in external ears, hands, feet, olecranon, and
prepatellar bursas; fever is common
2. LABS: Serum uric acid is elevated (normal in 25%), CBC,
sedimentation rate, aspiration of affected joint, tophus, x-ray
XIII.
iv. DDx.: Cellulitis, acute pyogenic arthritis (exclude with bacteriologic
studies), chronic RA, chronic lead intoxication
v. Treatment: ACUTE: NSAIDs (NO aspirin), corticosteroids, analgesics
(for pain); BETWEEN ATTACKS: Diet (low purine diet (high purine:
meats, yeasts, some vegetables), weight loss, decrease alcohol); low dose
colchicines; allopurinol
vi. Prognosis:
d. Crystal Deposition Arthritis (Chondrocalcinosis and pseudogout)
Autoimmune Disease
a. Rheumatoid Arthritis
i. Essentials of Diagnosis
1. Prodromal systemic symptoms of malaise, fever, weight loss, and
morning stiffness
2. Onset is usually insidious and in small joints; progression is
centripetal and symmetric; deformities common
3. Radiographic findings: juxta-articular osteoporosis, joint erosions,
and narrowing of the joint space
4. Rheumatic factor is usually present
5. Extra-articular manifestations: subcutaneous nodules, pleural
effusions, pericarditis, lymphadenopathy, splenomegaly with
leucopenia, and vasculitis
ii. Clinical Findings:
1. S/S: Prodromal symptoms: malaise, weight loss, and vague
periarticular pain or stiffness; symmetric joint swelling with
associated stiffness, warmth, tenderness, and pain; Stiffnes >30
min in morning (better throughout the day)
2. LABS: Rhematic factor, ANA, CBC; radiograph
iii. DDx.: Rheumatic fever, SLE, osteoarthritis, gout, septic arthritis
iv. Treatment: Education, physical and occupational therapy, systemic rest,
articular rest, exercise, heat and cold, assistive devices, splints, weight
loss; NSAIDS, TNF-α inhibitors, Methotrexate, CST
v. Course and Prognosis
b. Systemic Lupus Erythematosus
i. Essentials of Diagnosis
1. Occurs mainly in young women
2. Rash over areas exposed to sunlight
3. Joint symptoms in 90% of patients. Multiple system involvements
4. Depression of hemoglobin, WBC, and platelets
5. Serologic findings: ANA, anti-ds DNA ab, low serum complement
levels
ii. Clinical Findings
1. S/S: Fever, anorexia, malaise, and weight loss. Skin lesions
(butterfly rash), alopecia, joint symptoms; LABS: CBC, ANA,
anti-ds DNA, complement levels
2. 4 of the following 11 criteria: Malar rash, discoid rash,
photosensitivity, oral ulcers, arthritis, serositis, renal disease,
neurologic disease, hematologic disorders, immunologic
abnormalities, positive ANA
iii. Treatment: Supportive care, rest, NSAIDs, CST
XIV. Headaches: Intensity, quality and site of pain
a. Tension HA:
i. S/S: Poor concentration, daily, tight in quality, exacerbated by emotional
stress, fatigue, noise or glare. HA are generalized and may be most tense
about the neck or back of the head
ii. Tx: NSAIDs, antimigrainous agents, relaxation techniques
b. Depression HA:
i. S/S: Worse than tension HA, arise in the morning, accompany depression
ii. Tx: Anti-depressants
c. Migraine:
i. S/S: Lateralized throbbing HA, can be generalized. Associated with
anorexia, nausea, vomiting, photophobia, phonophobia, and blurring of
vision. Usually have triggers, follow a prodrome and persist for hours
ii. Tx.: Avoid triggers, during attack rest in quiet, dark room, NSAID, or
anti-migraine medication
d. Cluster HA:
i. S/S: Middle-aged men; severe uni-lateral periorbital pain occur daily for
several weeks; accompanied by ipsilateral nasal congestion, rhinorrhea,
lacrimination, redness of eye, and Horner’s syndrome; occur at night,
awaken the patient, and last for < 2 hours; Spontaneous remission; have
triggers
ii. Tx: Subcutaneous sumatriptan to treat current attack; Ergotamine tartrate
as rectal suppository for prophylaxis therapy (also can use propranolol,
lithium carbonate, prednisone)
e. Giant Cell (Temporal or cranial) Arteritis
i. S/S: Elderly; HA associated with myalgia, malaise, anorexia, weight loss;
complication: loss of vision; exam reveals tenderness of scalp and over
temporal arteries
ii. Tx: Biopsy, further tx in chapter 20
f. Posttraumatic HA
i. S/S: Appears within a day following injury; worsen over the ensuing week
and then subside; described as a constant dull ache with superimposed
thrombing; may be accompanied by nausea, ,vomiting, or scinitillating
scotomas; disequilibirium, impaired memory, poor concentration,
emotional instability; CT scan is normal
ii. Tx.: Encouragement and graduated rehab, HA may respond to NSAIDs
g. Cough HA
i. S/S: Last only a few minutes following coughing; GET A CT: rule out
Arnold-chiari or some space occupying lesion
ii. Tx.: Sometimes clear after lumbar puncture, indomethacin may provide
relief
h. HA due to intracranial mass lesions
XV.
i. S/S: Dependent of location; non-specific (mild-severe); may worsen with
exertion or postural change; associated with nausea and vomiting; GET
CT scan
i. HA due to other neurologic cause
CVA
a. Transient Ischemic Attacks
i. Essentials of Diagnosis
1. Focal neurologic deficit of acute onset
2. Clinical deficit resolves completely within 24 hours
3. Risk factors for vascular disease often present
ii. General considerations: 30% of people with stroke have history of TIA;
risk of stroke is highest in the one month following TIA
iii. Etiology: From embolization; Subclavian Steal Syndrome – transient
vertebrobasilar ischemia, localized stenosis or occlusion of one subclavian
artery proximal to the source of the vertebral artery
iv. Clinical Findings:
1. S/S: Vary between people, remain constant in an individual; abrupt
onset followed by complete recovery;
a. Carotid artery: weakness and heaviness of contralateral
arm, leg, or face; can also see numbness or paresthesias;
slowness of movement, dysphagia, or monocular visual
loss in eye contralateral to limbs affected; Exam: flaccid
weakness, sensory changes, hyperreflexia, positive babinski
response, dysphagia
b. Vertebrobasilar: Vertigo, ataxia, diplopia, dysarthria,
dimness or blurring of vision, perioral numbness and
paresthesias, and weakness or sensory complaints on one,
both, or alternating sides of body
2. Imaging: CT scan, MR angiography
3. Labs: Assessment for HTN, heart disease, hematologic disorders,
DM, hyperlipidemia, and peripheral vascular disease; CBC, fasting
blood glucose and serum cholesterol and homocysteine
determinations, serologic tests for syphilis, and ECG and CXR
v. DDx.: Focal seizures, classic migraine, focal neurologic deficits during
periods of hypoglycemia in DM
vi. Treatment: Operative treatment if angiogram reveals focal high grade
stenosis; stop smoking; anticoagulation therapy with Heparin followed by
Warfarin; Treat underlying cause
b. Stroke
i. Essentials of diagnosis
1. Sudden onset of characteristic neurologic deficit
2. Patient often has history of HTN, DM, valvular heart disease, or
atherosclerosis
3. Distinctive neurologic signs reflect the region of brain involved
ii. Lacunar infarction:
1. Small lesions that occur in the basal ganiglia, pons, cerebellum,
anterior limb of internal capsule
2. Due to HTN; cause pure sensory deficit, ipsilateral ataxia with
crural paresis, and dysarthria with clumisness of hand; CT
iii. Cerebral infarction: thrombotic or embolic occlusion
1. Clinical findings:
a. Carotid circulation
i. Opthalmic: Sudden, brief loss of vision in one eye
ii. ACA: Weakness and cortical sensory loss in
contralateral leg; contralateral grasp reflex,
paratonic rigidity, and abulia or frank confusion
iii. MCA: Contralateral hemiplegia, hemisensory loss,
and homonymous hemianopia (eyes deviate toward
side of lesion); global aphasia
b. Obstruction of vetebrobasilar circulation
i. PCA: Thalamic syndrome, spontaneous pain and
hyperpathia; macular sparing hemianopia
ii. Veterbral artery: May be clinically silent; if both, or
basilar: coma with pinpoint pupils, flaccid
quadriplegia and sensory loss, and variable cranial
nerve abnormalities
iii. Cerebellar arteries: Vertigo, nausea, vomiting,
nystagmus, ipsilateral limb ataxia, and contralateral
spinothalamic sensory loss in limbs
c. Imaging: CT scan in first 48 hours
d. Labs: CBC, sedimentation rate, blood glucose, serologic
test for syphilis, ANA levels, lipid panel, ECG
2. Treatment: Thrombolytic therapy if within first 3 hours;
anticoagulants, heparin followed by warfirin; Physical therapy
3. Prognosis
iv. Intracerebral hemorrhage
1. Clinical findings
a. S/S: Usually due to HTN; initial loss of consciousness;
vomiting, HA; further signs depend on location
b. Imaging: CT scan without contrast
c. Labs: CBC, platelet count, bleeding time, PPT and aPPT,
liver and renal function test; NO lumbar puncture
2. Treatment: Neurologic management is conservative and
supportive;
v. Subarachnoid hemorrhage (often associated with aneurysm or AVM)
1. Essentials of Diagnosis:
a. Sudden severe HA
b. Signs of meningeal irritation usually present
c. Obtundation is common
d. Focal deficits frequently absent
2. Clinical findings
a. S/S: Sudden, very severe HA followed by nausea and
vomiting; loss of consciousness; if consciousness is
regained, confused and irritable, altered mental status;
EXAM: Nuchal rigidity
b. Imaging: CT scan immediately
3. Treatment: Confined to bed, advised against exercise or straining,
treated symptomatically for HA and anxiety, given laxatives and
stool softeners; IF hyptertensive, slowly lower BP; Phenytoin to
prevent seizures
vi. Intracranial Aneurysm
1. Clinical findings: Usually asymptomatic until they rupture, then
present as subarachnoid hemorrhage; can have warning leak; SEE
ABOVE FOR LABS AND IMAGING + angiography and lumbar
puncture
2. Treatment: Surgical intervention to prevent further ruptures +
treatment for subarachnoid hemorrhage
vii. Arteriovenous Malformations
1. Clinical findings
a. Supratentorial: Most are supratentorial; hemorrhage,
recurrent seizures, HA, and focal deficits; generally bleed
before the age of 40; cranial bruits (best heard over the
ipsilateral eye or mastoid region)
b. Infratentorial: Clinically silent, may hemorrhage, cause
hydrocephalus or lead to progressive and relapsing brain
stem deficits
c. Imaging: CT scan, angiography, MRI
d. Labs: CSF examination
2. Treatment: Surgical intervention: either removal or emboliation
viii. Intracranial venous thrombosis
c. Spinal cord vascular disease
i. Essentials of diagnosis
1. Sudden onset of back or limb pain and neurologic deficit in limbs
2. Motor, sensory, or reflex changes in limbs depending on level of
lesion
3. Imaging studies distinguish between infarcts and hematoma
ii. Infections of the spinal cord: Rare; only occurs in territory of anterior
spinal artery; acute onset of flaccid, areflexive paraplegia  spastic
paraplegia with extensor plantar responses; dissociated sensory loss
(preservation of vibration and position) Tx.: Symptomatic
iii. Epidural or subdural hemorrhage: Sudden severe back pain followed by
acute comprehensive myelopathy
iv. Arteriovenous malformation of the spinal cord: Congenital; present with
spinal subarachnoid hemorrhage or myeloradiculopathy; motor and
sensory disturbances in legs or arms and to sphincter disorders; EXAM:
upper, lower, or mixed motor deficit in legs, sensory deficits; IMAGING:
Myelography, spinal arteriography; TRETMENT: ligation of vessels