Sweep 3

Question 1

• posterior lobe (pituitary): composed of

Answer 1

modified glial cells and axonal processes extending from hypothalamic neurons

Question 2

B. Hypofunction (hypopituitarism)
o ———–, most commonly from Sheehan’s syndrome (postpartum infarct). Need over 75% of anterior lobe to be destroyed for clinically significant effects.

Answer 2

Ischemic necrosis

Question 3

B. Hypofunction (hypopituitarism)

• manifestations

Answer 3

o No post-partum lactation (prolactin)

Question 4

II. Hyperthyroidism

Graves’ Disease

Answer 4

• autoimmune, significant genetic component

o Autoantibodies to TSH receptor; constantly stimulated

Question 5

Papillary Thyroid Carcinoma

Answer 5

o Many have mutations in the RET proto-oncogene
o Pathology
o microscopically characterized by papillary projections
o distinctive nuclear changes
o nuclear clearing, aka “orphan annie nuclei”
o nuclear grooves
o nuclear inclusions
o nuclear enlargement

Question 6

Follicular Carcinoma

Answer 6

o Must see invasion through the capsule or into the blood vessels

Question 7

o Nodular glomerulosclerosis

Answer 7

• 15-30% of long-term diabetics; specific to diabetics
• Ball-like deposition of matrix at the periphery of the glomerulus
• Total renal failure
• Renal atherosclerosis
• Pyelonephritis

Question 8

• Diabetic neuropathy

Answer 8

o Autonomic neuropathy causing disturbances in bowel and bladder function, impotence

Question 9

Reactive arthritis =

Answer 9

chlamydia

Question 10

Hyperaldosteronism

• Characterized by

Answer 10

chronic excess aldosterone secretion – causes:
o Sodium retention, Potassium excretion
o Hypertension and hypokalemia

Question 11

Hyperaldosteronism

• Secondary

Answer 11

o Aldosterone release in response to activation of renin-angiotensin system
o Increased levels of plasma renin

Question 12

Primary Chronic Adrenocortical Insufficiency (Addison’s Disease)

Answer 12

• Progressive destruction of adrenal cortex
• Serum ACTH may be elevated → skin and mucosal pigmentation
• Destruction of cortex prevents response to ACTH
• Potassium retention, sodium loss, hyperkalemia, hyponatremia, volume depletion, and hypotension

Question 13

Secondary Adrenocortical Insufficiency

Answer 13

• Any disorder of hypothalamus of pituitary that reduces output of ACTH
• Symptoms similar to Addison’s disease
o But no skin/mucosa pigmentation

Question 14

3. Subarachnoid hemorrhage

Answer 14

a. Often are spontaneous, but could also be precipitated by traumatic injury.
b. Chief complaint of patient “Worst headache of my life”.
c. Ruptured berry (saccular) aneurysm (of major brain arteries) is the most common cause of non-traumatic hemorrhage.

Question 15

Primary hyperparathyroidism

Answer 15

“painful bones, renal stones, abdominal groans, and psychic moans

Question 16

B. Cholecystitis

Answer 16

1. May be acute or chronic, 4th – 6th decades, F > M
2. Almost always occurs in association with gallstones
3. Note upper right quadrant pain, may note low level fever, anorexia, tachycardia, nausea, vomiting. Acute symptoms-can arise very abruptly.
4. Chronic-not as dramatic a presentation. Note recurrent bouts of colicky epigastric or right quadrant pain.
   • Vague symptoms, Stones (90 %), Fibrosis & Inflammation

Question 17

8. Encephalitis.

Answer 17

a. Diffuse inflammation of the brain parenchyma caused by a number of viral agents e.g. HSV most common, HIV, cytomegalovirus and also many arthropod-borne encephalitis viruses.
b. Clinical symptoms: headache, neck stiffness, pyrexia (fever) and focal seizures.
c. Without treatment, usually fatal.
d. Microscopically can note perivascular lymphocytosis, microglial nodules and neuronophagia. May also note viral inclusions e.g. Cowdry A and Negri bodies.

Question 18

Ependymoma.

Answer 18

a. Well-circumscribed lesions, arising from ventricular wall. Elongated cells with processes radiating around blood vessels (perivascular pseudorosettes)

Question 19

4. Hemochromatosis.

• . Classic triad:

Answer 19

cirrhosis with hepatomegaly, diabetes mellitus, and skin pigmentation.

Question 20

2. Primary biliary cirrhosis (PBS)

Answer 20

a. Inflammatory autoimmune disease-affects intrahepatic bile ducts.
b. Primary feature-nonsuppurative inflammatory destruction of medium sized intrahepatic ducts-also get portal inflammation, scarring and eventually cirrhosis.
c. Thought to be an autoimmune etiology.

Question 21

2. Primary sclerosing cholangitis (PSC)

Answer 21

a. Fibrosing cholangitis of bile ducts-develop luminal obliteration
b. Liver eventually develops biliary cirrhosis
c. NOTE: same common endpoint i.e. biliary cirrhosis as primary and secondary biliary cirrhosis
d. Note an increase in chronic pancreatitis and hepatocellular carcinoma (HCC) in PCS patients

Question 22

C. Cirrhosis

3. Morphologic changes are:

Answer 22

1) bridging fibrous septa, 2) parenchymal nodules, 3) changes in architecture, with parenchymal injury and scarring as the end result. A fibrotic liver has a markedly compromised blood supply and decreased function.

Question 23

Urticaria:

Answer 23

Hives CLINICAL FEATURES
• Erythematous, edematous, and pruritic papules and plaques (wheals)
• Individual hives last <24 hours (just a few hours), but episodes can continue for weeks
• Localized or generalized