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Endo/Repro Flashcards

0
Q

Mech of glucose as insulin stimulator

A
  1. Glucose into cell, metabolized –> ATP
  2. ATP => close K+ channels -> depolarize
  3. open volt-gated Ca2+ channels –> Ca2+ influx => insulin secretion
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1
Q

Glucose Receptor types:
GLUT-1
GLUT-2
GLUT-4

A

1: insulin INdependent (RBCs, brain)
2: BIdirectional (B islet cells, liver, kidney, small intestine)
4: insulin DEpendent (fat, skeletal muscle)

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2
Q

Effects of insulin (on ALL parts of body!) “anabolic”

A
  1. skel. m/fat: increase glucose uptake, increase protein synthesis
  2. liver: increase glycogen synthesis, and TG synthesis/storage
  3. kidneys: increase Na+ retention
  4. increase cell uptake of K+ & AAs
  5. decrease glucagon release
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3
Q

Effect of adrenergic signalers on insulin secretion

A

B2 antagonists: increase insulin

Alpha2 agonists: decrease insulin

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4
Q

3 types of pancreatic cells

A
  1. alpha –> glucagon
  2. beta –> insulin
  3. delta –> somatostatin *inhibits glucagon and insulin secretion
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5
Q

regulation of growth hormone (“somatotropin”)

A

secretion = in pulses, increases during exercise and sleep

Inhibitors: glucose, somatostatin

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6
Q

Case:

Child with hypertension, hypokalemia and ambiguous genitalia/lack of secondary sex characteristics

A

congenital bilateral adrenal hyperplasia (CAH), w/ 17a hydroxylase def.
=> high mineralcorticoids, low cortisol and sex hormones
Male: undescended testes, ambig. genitalia (insuff. DHT)
Female: normal int. & external sex genitalia, no secondary sex features

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7
Q

Case:

young female with hypotension, hyperkalemia, increased renin activity & volume depletion, and pseudohermaphroditism

A

CAH (congenital adrenal hyperplasia) w/ 21-hydroxylase def.
*most common form of CAH
low mineralcorticoids & cortisol, high sex hormone levels
–> masculinization bc shunting of products towards testosterone

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8
Q

Case:

Young adult female with hypertension and masculinization

A

CAH (congenital adrenal hyperplasia) w/ 11B-hydroxylase def.
=> low aldosterone! but high 11-deoxycorticosterone, low cortisol, HIGH sex hormone levels
Masculinization bc shunt products toward testosterone

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9
Q

major functions of cortisol (4)

A
  1. maintain BP (upregulate a1 Rs in arterioles)
  2. inhibit Bone formation & fibroblasts
  3. Immune-suppression/anti-inflam. (–l leukotrienes, prostaglandins, histamine, eosinophils, IL-2, and leuk adhesion)
  4. Increase Gluconeogenesis and insulin resistance
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10
Q

function of PTH (parathyroid hormone)

A

Goal: increase serum Ca2+

  1. increase bone reabsorption
  2. increase renal reabsorption of Ca2+ & decrease renal PO4- reabs.
  3. increase 1,25-D3 production (stimulate renal 1a-hydroxylase)
    * opposed by calcitonin*
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11
Q

effect of 1,25D3 on gut absorption

A

active Vit D (1,25D3 aka calcitriol) acts on gut to increase Ca2+ AND PO4- absorption!
(vs PTH acts on kidney, increases Ca reabs. & decreases PO4- reabs.)

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12
Q

Function of T3 (thyroid hormone)

“4 B’s”

A
  1. Brain maturation
  2. Bone growth
  3. B1 adrenergic (increase CO, HR, SV, contractility)
  4. increase Basal metabolic rate (via Na+/K+ ATPase –> incr. O2 consumption, RR, body temp; also incr. glycogenolysis/gluconeogen.)
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13
Q

Wolff-Chaikoff effect

A

excess iodine in system –> temporarily inhibits thyroid peroxidase
=> less iodine processing = less T3 & T4 production

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14
Q

Distinguishing between types of abnormal ACTH secretion

Cushing’s syndrome

A

use dexamethasone suppression test (low and high dose)…
normal: cortisol suppressed by low OR high dose.
Pituitary adenoma: high ACTH, low - elevated, high - suppressed.
Ectopic tumor: high ACTH, low - elevated, high - still elevated.
Cortisol tumor (adrenal): less ACTH, low - elevated, high - elevated.

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15
Q

symptoms of Cushing’s disease/syndrome

A

HTN, weight gain, truncal obesity and buffalo hump, hyperglycemia, stria/thin skin, osteoporosis, amenorrhea, immune suppression

16
Q

Conn’s syndrome

A

aldosterone-secreting adrenal adenoma (primary hyperaldosteronism)
=> HTN, hypOK+, metabolic alkalosis, low plasma renin
Tx: spironolactone and/or surgical resection

17
Q

primary vs. secondary hyperaldosteronism

A

Primary: too much aldosterone (adrenal hyperplasia or ectopic)
=> LOW plasma renin
Secondary: overactive RAAS bc kidneys percieve low volume
=> HIGH plasma renin level (ie: renal a stenosis, CHF, cirrhosis, etc)

18
Q

Primary vs. Secondary adrenal insufficiency

A

Primary (Addison’s disease): adrenal destruction bc disease process
=> hypotension, hyperK+, acidosis, skin hyperpigmentation (bc MSH)

Secondary: NO skin hyperpigmentation or hyperK+

19
Q

Case:
Child with swollen belly & diarrhea, also generalized fatigue, etc. Testing shows increased HVA (Homovanillic acid) in urine.

A

= Neuroblastoma (of adrenal medulla/sympathetic chain)

  • over-expression of n-myc => risk rapid tumor progression
  • similar to pheochromocytoma but HTN less likely
20
Q

Types of hypOthyroidism

A

1: Hashimoto’s: autoimmune, w/ HLA-DR5 & anti-thyroiglobulin Abs

  1. congenital (Cretinism): hypotonic, poor feeding, umbilical hernia
  2. Subacute/DeQuervain’s: post-flu, self limited w/ granulomatous inflamm. Very tender thyroid.
  3. Riedel’s: replace thyroid w/ fibrous tissue, “rock hard” & immobile.
21
Q

types of hypERthyroidism

A
  1. Toxic/Multinodular goiter: focal “hot nodules” bc TSH R mutation
  2. Grave’s disease: IgG Ab to TSH R (“thyroid-stimulating globulins”), w/ diffuse goiter.
    * complication:
    Thyroid storm…catecholamine surge -> arrhythmia -> death *high AlkP
22
Q

Common presentations for pituitary adenoma

A

1: prolactinoma –> amenorrhea, galactorrhea, bitemporal hemianopia. Tx = bromocriptine (dopamine agonist)

  1. Acromegaly (excess GH)
    * Dx: GH doesn’t suppress w/ oral glucose tolerance test
23
Q

Diabetes Insipidus: nephrogenic vs. central

A

=> LOW urine specific gravity (can’t [ ] urine), polydipsia/polyuria.
Nephrogenic DI: no rxn to ADH => does NOT correct w/ desmopressin
Central DI: lack ADH => DOES correct w/ desmopressin

24
Q

Diabetes Insipidus vs. psychogenic polydipsia

A

BOTH have polydipsia & polyuria. Use water deprivation test:
DI: urine osmolarity does NOT increase w/ deprivation (can’t [ ])
=> for DI do NOT limit H2O (will become hypovolemic)
Psychogenic: urine DOES [ ] over time w/ deprivation

25
Q

Diabetes Insipidus & Psychogenic polydipsia vs. SIADH

A

DI & psychogenic polydipsia: polydipsia & polyuria, LOW urine [ ]
SIADH: high urine output w/ [ ] > serum, corrects w/ water restriction
(abnormal water retention => hyponatremia bc excrete Na+)
=> confusion, other non-specific symptoms. Coma if severe.

26
Q

LH vs. FSH in female

A

LH => stimulates ovulation (rapid peak in levels)
FSH: stimulates ovarian follicle to make estrongen =>increase FSH Rs
–> endometrial proliferation

27
Q

progression of progesterone synthesis in ovulation & pregnancy

A
  1. Granulosa cells of follicle (estrogen before ovulation, progesterone after) *Granulosa cells become corpus luteum
  2. corpus luteum/embryo
  3. placenta (@ wk 5-9)
28
Q

Effect of estrogen on cholesterol levels

A

HDL increases & LDL decreases w/ estrogen

29
Q

General effects of progesterone

A

Goal: prepare for/maintain pregnancy (after ovulation)

  • induce/maintain corpus luteum (-> spiral aa, etc.)
  • thickens cervical mucus (prevent sperm entry)
  • relax uterine smooth muscle
  • increase body temp
30
Q

Tanner stages of sexual development

A 
I - childhood
II - pubic hair appears ("thelarche")
III - penis lenghtens/breast enlargement
IV - increase penis girth, raised areolae
V - adult (areolae not raised)
31
Q

Histological evidence of Ectopic pregnancy

A

decidualized endometrium w/ no chorionic villi on endometrial biopsy
(implantation in Fallopian tubes => fail to dvp fully)
Sx = pain (esp. sudden, lower abdominal) +/- bleeding

32
Q

polyhydramnios vs. oligohydramnios

A

Polyhydramnios: too much fluid => anencephaly
(esophageal/duodenal atresia => can’t swallow fluid)
Oligohydramnios: too LITTLE fluid => Potter sequence (face deformity)
(placental insuff, bilat renal agenesis, post. urethral valves (Male)
–> can’t excrete urine)

33
Q

Types of ovarian cysts (5)

A

1: Follicular cyst: UNruptured follicle, +/- endometrial hyperplasia

  1. Endometrioid cyst: endometriosis in ovary *bleeds w/ menses
  2. Theca-Lutein cyst: >1/bilat., from LH/FSH stim., risk choriocarc.
  3. Dermoid cyst: teratoma (mature)
  4. Corpus luteum cyst: persistent corpus luteum w/ hemorrhage
34
Q

Types of gonadal germ cell tumors

A

1: Teratoma: *mature = benign in F, immature always malignant

  1. Yolk sac tumor: malign, yellow solid mass, “glomeruloid,” high AFP
  2. Dysgerminoma/Seminoma: high hCG, sheets of uniform cells
    *4. Choriocarcinoma: = trophoblast -> only in mom or baby, high hCG
    => early hematog. mets to lungs
35
Q

Benign breast masses (5)

A 
# 1. Fibroadenoma (esp.  nipple discharge
5. Phyllodes tumor: large & bulky (CT & cysts), esp. 60s
36
Q

5 types of Malignant Breast cancer

A

1: Invasive ductal (worst): firm, fibrous, “stellate”

  1. Invasive Lobular: bilateral, orderly
  2. Medullary: fleshy w/ lymphocytic infiltrate
  3. Inflammatory: dermal lymphatic invasion, block => “peau d’orange”
  4. DCIS = Ductal carcinoma In Situ/Comedocarcinoma
    • Paget’s disease = sign of DCIS
37
Q

Direct vs. Indirect vs. Femoral hernia

A
  • Direct: Hesselbach’s triangle, w/ inferior epigastric vessels LATERAL, and rectus abdominus medial.
  • INdirect (#1 M): INternal inguinal ring, w/ inf. epigastrics MEDIAL.
  • Femoral (#1 F): femoral canal, w/ femoral v. lateral & Cooper’s ligament posterior.
    • Femoral = below inguinal ligament & lat. to pubic tubercle*
38
Q

CAH vs. Aromatase deficiency

A

CAH (congen. adrenal hyperplasia): F ambig. genitalia & Na+ wasting
= 21-hydroxylase def.
Aromatase def: F ambig. genitalia, tall, & virilize mom during pregnancy
=> failure to convert androstenedione & testosterone to estriol/estrone

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