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Flashcards in Sweep 3 Deck (23):

- posterior lobe (pituitary): composed of

modified glial cells and axonal processes extending from hypothalamic neurons


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.

Ischemic necrosis


B. Hypofunction (hypopituitarism)
• manifestations

o No post-partum lactation (prolactin)


II. Hyperthyroidism
Graves’ Disease

• autoimmune, significant genetic component
o Autoantibodies to TSH receptor; constantly stimulated


Papillary Thyroid Carcinoma

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


Follicular Carcinoma

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


o Nodular glomerulosclerosis

• 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


• Diabetic neuropathy

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


Reactive arthritis =



• Characterized by

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


• Secondary

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


Primary Chronic Adrenocortical Insufficiency (Addison’s Disease)

• 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


Secondary Adrenocortical Insufficiency

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


3. Subarachnoid hemorrhage

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.


Primary hyperparathyroidism

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


B. Cholecystitis

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


8. Encephalitis.

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.



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


4. Hemochromatosis.
• . Classic triad:

cirrhosis with hepatomegaly, diabetes mellitus, and skin pigmentation.


2. Primary biliary cirrhosis (PBS)

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.


2. Primary sclerosing cholangitis (PSC)

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


C. Cirrhosis
3. Morphologic changes are:

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.



• 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