Pathology Flashcards
(28 cards)
What cells are hyperproliferative in medullary carcinoma of the thyroid? What mutation is it associated with?
Parafollicular “C” cells that produce calcitonin
sheets of cells in amyloid stroma
RET mutation
MEN 2A and 2B syndromes
Pt with persistant diarrhea, weight loss, abdominal pain refractory to medical therapy with duodenal and jejunal ulcers?
Gastrinoma!
neuroendocrine tumor most commonly in pancreas, peripancreatic tissue, or duodenum
high levels of acid secretion and ulcers (often in unusual places)
jejunal ulcers = highly suggestive of gastrinoma!
What is pituitary apoplexy?
acute hemorrhage into preexisting pituitary adenoma
bimodal symptoms - acute (severe headache and CN palsies) with chronic symptoms of pituitary tumor
risk of cardiovascular collapse from adrenocortical insufficiency (low ACTH)
Thyroid cancer with psamomma bodies? What other distinguishing features? Mutations?
papillary carcinoma
Orphan Annie eye nuclei, ground-glass nuclei with grooves
associated with RET and BRAF mutations, childhood radiation
Pt with scrotal mass and high T4/T3?
hCG peptide hormone similar in structure to TSH, LH, and FSH
can bind TSH receptor (although with much lower affinity than TSH)
Most likely from a teratoma (non-seminomatous germ cell tumor), but also seen in small percentage of seminomas
What are seen in the islets of Type I diabetics? Type II?
Type I: lymphocytic infiltrate
Type II: deposition of islet amyloid polypeptide (IAPP)
Which congenital adrenal enzyme deficiencies present with enlargement of the adrenal glands?
ALL the congenital adrenal enzyme deficiencies are characterized by adrenal cortical hyperplasia / enlargement of BOTH adrenal glands due to increased ACTH stimulation (due to decreased cortisol in all 3!!)
ALL have decreased cortisol levels!
What is the treatment of congenital adrenal hyperplasia?
administration of low (i.e. physiologic) doses of exogenous corticosteroids to suppress ACTH secretion
androgen production by the adrenal cortex will decrease in response to removal of excessive ACTH (all 3 disorders have a cortisol deficiency)
What effect does hydrochlorothiazide have on serum calcium levels and PTH?
increases the distal tubular reabsorption of filtered calcium
INCREASED serum calcium and subsequent suppression of PTH
Anorexia nervosa signs and labs?
low levels of LH, FSH, estradiol, and estrone
(hypogonadotropic amenorrhea)
- distorted body image
- inadequate diet
- regular exercise while underweight
- dry skin
- lanugo hair (fine, downy hair)
Pt with shock in combination with hyponatremia, hyperkalemia, and hypoglycemia?
strongly suggestive of adrenal crisis!
Pt with fever, vomiting, nuchal rigidity, and petechial rash?
strongly suggestive of meningococcal meningitis!
Neisseria meningitidis septicemia with adrenal hemorrhage?
Waterhouse-Friderichsen syndrome
Pt with generalized weakness and paresthesias, high BP, very low renin - what are her Na+, K+, and HCO3- levels?
normal Na+
low K+
high HCO3-
pt has primary mineralocorticoid excess
HTN and low renin due to too much aldosterone
weakness and paresthesias due to alkalosis
mineralocorticoid excess leads to:
- sodium retention (but normal serum Na+)
- potassium loss (low K+)
- increased urinary H+ excretion (high bicarb)
Hypernatremia is rare due to aldosterone escape!
Aldosterone escape - process by which increased Na and Cl absorption leads to intravascular hypervolemia, which in turn promotes the release of atrial natriuretic peptide (ANP) to cause diuresis and eventual compensatory sodium loss.
Thus, no edema but do have HTN due to mild volume expansion.
What is aldosterone escape?
process by which increased Na and Cl absorption leads to intravascular hypervolemia, which in turn promotes the release of atrial natriuretic peptide (ANP) to cause diuresis and eventual compensatory sodium loss.
Thus, no edema but do have HTN due to mild volume expansion.
What is the most preferred way to screen pts for diabetes mellitus? Common presentation for Type I pt?
fasting blood sugar is the most preferred way to screen pts
Type I: sometimes history of viral infection, often young Caucasian adult
What are Hurthle cells associated with? Genetic association?
Hashimoto’s
germinal centers
HLA-DR5
enlarged, NONTENDER thyroid
What are craniopharyngiomas derived from? Location? Components? Symptoms?
suprasellar tumors arising from remnants of Rathke’s pouch
solid, cystic, calcified (all three = highly suggestive!)
headaches, visual field defects, hypopituitarism
present during childhood
Rule of 10s for pheochromocytoma?
10% bilateral malignant extra-adrenal kids calcify occur as part of hereditary syndromes (MEN2A, 2B, von Hippel Lindau)
Pt with jaw pain, elevated ESR, diffuse decrease in radioactive iodine uptake? Histological findings and prognosis?
subacute thyroiditis / de Quervain / granulomatous
granulomatous inflammation and giant cells seen
self-limited, responds to NSAIDs
What is macrosomia and why does it occur in children exposed to gestational diabetes? What might be expected after delivery?
Macrosomia - large infant
associated with poor glucose control during pregnancy
high insulin levels = increased fat deposition and enhanced fetal growth
high glucose levels in mother enter fetal circulation – fetus responds by increasing insulin production (maternal insulin is NOT transferred to fetus because it is catabolized during transfer to placenta)
after birth, neonate continues to overproduce insulin, potentially causing severe hypoglycemia (transient)
Neonatal complications of diabetes during pregnancy?
- premature delivery
- macrosomia
- neural tube defects
- hypoglycemia
- hypocalcemia
- polycythemia
- respiratory distress
- transient hypertrophic cardiomyopathy
Pt with episodic sudden onset headache, heart palpitations, apprehensiveness, diaphoretic, tremor?
pheochromocytoma
episodic release of catecholamines!
Pt with diabetes mellitus, necrolytic erythema, and anemia?
Glucagonoma
necrolytic erythema - elevated erythematous rash
