Block 7

Front 1

Are islet autoantibodies involved in the destructive process of beta cells in T1DM?

Back 1

Islet autoantibodies are not thought to be involved in the destructive process, but rather are formed as a result of β-cell destruction, and serve as immunologic markers.

Front 2

When is tight glycemic control used and not used?

Back 2

Use it to slow progression to renal dz and other macrovascular disease
Once CAD begins = don't

Front 3

Amylin vs Incretin effects?

Back 3

Amylin deficiency in T1DM
Actions: Inhibition of gastric emptying, inhibition of glucagon secretion (glucagon --> hepatic effects, MSK glycogen production)

Incretin deficiency in T2DM
Actions: Augment glucose-stimulated insulin secretion, suppress hepatic glucose output, slow gastric emptying, act centrally to enhance satiety

vs Amylin: not as broad effect vs glucagon, but acts directly to affect satiety

Front 4

What are the interplays between the cortisol axis and the RAAS system?

Back 4

ACTH, a pituitary peptide, also has some stimulating effect on aldosterone probably by stimulating the formation of deoxycorticosterone, a precursor of aldosterone.[16]

MR: The receptor is activated by mineralocorticoids such as aldosterone and deoxycorticosterone as well as glucocorticoids, like cortisol. In intact animals, the mineralocorticoid receptor is "protected" from glucocorticoids by co-localization of an enzyme, 11ß-hydroxysteroid dehydrogenase type 2 (11ß-HSD2), that converts cortisol to inactive cortisone.

Front 5

How is aldosterone synthesis induced?

Back 5

1) increase in the plasma concentration of Angiotensin III, a metabolite of Angiotensin II

2) increase in plasma angiotensin II, ACTH, or potassium levels, which are present in proportion to plasma sodium deficiencies (The increased potassium level works to regulate aldosterone synthesis by depolarizing the cells in the zona glomerulosa, which opens the voltage-dependent calcium channels.) The level of angiotensin II is regulated by angiotensin I, which is in turn regulated by the hormone renin. Potassium levels are the most sensitive stimulator of aldosterone.

3) the ACTH stimulation test, which is sometimes used to stimulate the production of aldosterone along with cortisol to determine whether primary or secondary adrenal insufficiency is present (However, ACTH has only a minor role in regulating aldosterone production; with hypopituitarism there is no atrophy of the zona glomerulosa.)

4) plasma acidosis

5) the stretch receptors located in the atria of the heart. If decreased blood pressure is detected, the adrenal gland is stimulated by these stretch receptors to release aldosterone, which increases sodium reabsorption from the urine, sweat, and the gut. This causes increased osmolarity in the extracellular fluid, which will eventually return blood pressure toward normal.

6) adrenoglomerulotropin, a lipid factor, obtained from pineal extracts. It selectively stimulates secretion of aldosterone

Front 6

How do you test for medullary carcinoma? What can't you use, unlike other thyroid cancers?

Back 6

Serum calcitonin. Can't use iodine and TSH b/c it doesn't express NIS.

Front 7

Why can't you use midnight plasma cortisol to test for Pseudo Cushings?

Back 7

It follows circadian rhythm and is below 7.5mg/dL or normal at midnight.

Front 8

What does 11beta-hydroxysteroid DH do and where is it located?

Back 8

They turn cortisol into cortisone, inactivating it.

It is located in the skin, liver, and kidneys.

It is also located in the colon, sweat glands, salivary glands, placenta, adipose tissue, and CNS.

Front 9

What is a sestimibe scan?

Back 9

Technetium (99mTc) sestamibi (trade name Cardiolite) is a pharmaceutical agent used in nuclear medicine imaging.

Sestamibi imaging is correlated with the number and activity of the mitochondria within the parathyroid cells, such that oxyphil parathyroid adenomas have a very high avidity for sestamibi,

Front 10

What constitutes polyglandular autoimmune syndrome type 2?

Back 10

Addison's, Hashimoto's, T1DM

Front 11

What constitutes polyglandular autoimmune syndrome type 1?

Back 11

Addison's, Hypopara, asplenism --> candidasis

Front 12

What glandular problem causes anovulation?

Back 12

Hypothyroidism

Front 13

How does Cushing's Syndrome cause elevation in androgen?

Back 13

ACTH-secreting tumor (pituitary): ACTH increases cortisol and androgens and aldosterone.

Front 14

How does FFA inc blood pressure?

Back 14

The infusion of FFAs into the portal vein activates the sympathetic nervous system and elevates blood pressure in the animal model.

Front 15

How does EE help the endometrium? What is it found in?

Back 15

It provides staiblity. It is synthetic estrogen found in COC's.

Front 16

Why is EE added to COC?

Back 16

It has the best

Front 17

How does COC prevent ovulation?

Back 17

It acts on the central players, estrogen inh FSH and progestin inh LH.

Front 18

What are some of the useful benefits of COC?

Back 18

Regularizes oligomennorhea
helps dysmenorhea
dec acne
dec PID
dec anemia for heavy bleeders
dec ovarian and endometrial CA
dec perimenopausal symptoms

Front 19

Where do the risks of stroke in <35ug EE COC come from?

Back 19

Progestin

Front 20

What should the pt do if they missed 3 pills or started 3 days late on the OC?

Back 20

They should use contraception for 7 days, continue on with the packs. If it is in the third week, they should ignore the placebo and start new pack.

If this occurs in the first week w/ unprotected sex, emergency contraception should be considered.

Front 21

What is the definition of menopause?

Back 21

Cessation of menstruation for 12 months.

Front 22

What is the def of early perimenopause? What is considered late menopause and postmenopause?

Back 22

2-8 years before menopause. Late peri = 1 year after FMP. Postmenopause = period 1 year after menopause until death.

Front 23

What are the risks of giving estrogen HRT alone?

Back 23

Pancreatitis
Endometrial hyperplasia/CA
Ovarian CA?
Kidney stones
Breast/bleeding SEs
Stroke
Dementia
DVT

Front 24

What are the risks of giving estrogen+progestin HRT?

Back 24

Brst CA
Total CA
Pancreatitis
Kidney stones
Breast/bleeding SEs
CHD
Stroke
Dementia
DVT/PE
Gallbladder dz

Front 25

What are the benefits of giving estrogen HRT alone?

Back 25

Improves:
Vasomotor symptoms
Vaginal Atrophy
Breast CA incidence if stop after 5 yrs
MI
Osteoporosis

Front 26

What are the benefits of giving estrogen+progestin HRT?

Back 26

Improves:
Vasomotor symptoms
Vaginal Atrophy
Osteoporosis
Colon CA

Front 27

What cardiovascular changes occur during pregnancy?

Back 27

Inc total BV
Inc CO
Dec SVR (sys and dias) //easier placental blood delivery

Front 28

What CV SS during pregnancy mimic heart disease?

Back 28

Dyspnea
Reduced exercise tolerance
JV distension
Displaced PMI to left
Peripheral edema
S3 gallop
Systolic flow murmur
Cardiomegaly

Front 29

What respiratory changes occur during pregnancy?

Back 29

Inc O2 consumption
Inc tidal volume
Inc minute ventilation //driven by progesterone

Front 30

What respiratory SS during pregnancy mimic heart disease?

Back 30

Dyspnea
Respiratory alkalosis

Front 31

What renal changes occur during pregnancy?

Back 31

Inc renal plasma flow
Inc GFR

Front 32

What renal SS during pregnancy mimic respiratory dz?

Back 32

Urinary frequency
Dilation of urinary collecting system //susceptible to UTI
Dec BUN/Creat
Dec serum osmol
Dec Na, K, Ca

Front 33

What happens to the GI physiology during pregnancy?

Back 33

Dec peristalsis and GERD //progesterone relaxing SM

Dec gastric emptying and intestinal motility
Inc water resorption, portal venous pressure, constipation, hemorrhoids //GI mechanically obstructed by enlarging uterus

Impaired gallbladder emptying //inc biliary chol and cholelithiasis

Front 34

What are SS of GI physiology during pregnancy that may mimic liver dz?

Back 34

Spider angiomata
Palmer erythema
Dec serum albumin
Inc serum alkaline phosphatase (AST, ALT unchanged)
Inc serum cholesterol

Front 35

What hapens to hematologic physiology during pregnancy?

Back 35

Physiologic anemia //more plasma volume
Iron-def anemia //inc RBC volume
Hypercoagulability

Front 36

Which progesterone receptor is stronger and is an activator for progesterone? What happens to this ratio during pregnancy?

Back 36

PR-B. PR-A suppresses progesterone activity. More PR-A is expressed during pregnancy.

Front 37

What are the stages in normal parturition?

Back 37

Phase 0: Quiescence
Lack of gap junctions, progesterone
Phase 1: Activation
Uterine stretch, activation of fetal HPA axis
Phase 2: Stimulation
CRH expression
Functional progesterone withdrawal
Estrogen activation
Oxytocin
Prostaglandins
Common pathway: cervical ripening, uterine contractility, fetal/decidual membrane activation
Phase 3: Involution
Oxytocin

Front 38

What is the most common type of pituitary tumor (adenoma)?

Back 38

Prolactinoma

Front 39

HGPIN is a likely precursor of what type of CaP?

Back 39

Intermediate and high grade, but not low grade.

Front 40

What are the target actions of Testosterone?

Back 40

Front 41

What tissue resemblance is observed in Meckel's diverticulum?

Back 41

pancreatic, gastric, or small intestine

Front 42

What can be a complication of Meckel?

Back 42

B12 deficiency:
from Bacterial overgrowth, leads to ~pernicious anemia

Front 43

What do GI muscles have a tendency to do?

Back 43

Constrict, i.e. LES when there is achalasia (esp. primary in the absence of NO producing neurons--myenteric plexus) or HD (lack of myenteric plexus or submucosal neurons)

Front 44

What is the genetic defect in Hirschsprung disease?

Back 44

Absence of RET genes or ligand.

Front 45

Where is colonic diverticulosis more likely to occur?

Back 45

Left colon/sigmoid

Front 46

What part of the anatomy does ulcerative colitis affect?

Back 46

Less the right side, more the left side. Inflammation extends into mucosa and maybe submucosa with superficial ulcers.

Front 47

What part does Crohn's disease affect?

Back 47

Any part of GI tract, >% ileum. Lesions can skip; inflammation is transmural (through mucosa/submucosa) with non-necrotizing granulomas, ulcerations and fissures.

Front 48

Difference between Crohn's and UC?

Back 48

Front 49

Which GI cancer's prognosis is related to size?

Back 49

Pancreatic

Front 50

Which GI cancer uses T as a rating of invasion rather than size?

Back 50

Colon Ca

Front 51

Can you get odynophagia with ESCCa? What is the more common symptom associated with ESCCa?

Back 51

Yes, but dysphagia is more common.

Front 52

Which Gastric malignancy is the most aggressive?

Back 52

Diffuse-type (Bormann grade IV).

Front 53

What is defined as preterm? Very preterm?

Back 53

preterm = <37 wks, very preterm = <32 wks

Front 54

What does follicle development (including putting up LH-R) respond to?

Back 54

E2 and FSH