Week 10: Endocrine

Question 1

failure of feedback systems

Answer 1

may fail to funciton properly, may respond to inappropriate signals

Question 2

dysfunction of an endocrine gland

Answer 2

Inability to produce or obtain an adequate quantity of required hormone precursors
Inability to convert precursors to the active hormone
Excessive or inadequate hormone production

Question 3

target cell dysfunction

Answer 3

failure of target cell to respond to its hormone

Question 4

thyroid synthesizes and releases

Answer 4

calcitonin, thyroxine, and triiodothyronine

Question 5

hyperthyroidism clinical manifestations

Answer 5

increased metabolic rate with heat intolerance and increased tissue sensitivity to stimulation by the sympathetic nervous system, enlargement of thyroid gland

Question 6

hyperthyroidism tx

Answer 6

methimazole or propylthiouracil
radioactive iodine therapy
surgery

Question 7

causes of hyperthyroidism

Answer 7

graves disease
toxic multinodular goiter
toxic adenoma
follicular thyroid carcinoma
TSH secreting pituitary adenomas

Question 8

hyperthyroidism endocrine effects

Answer 8

goiter, bruit, diminished sensitivity to endogenous insulin

Question 9

hyperthyroidism reproductive effects

Answer 9

oligomenorrhea, erectile dysfunction

Question 10

hyperthyroidism GI effects

Answer 10

weight loss, anorexia, increased peristalsis, changes in vitamin metabolism

Question 11

hyperthyroidism integumentary effects

Answer 11

excessive sweating, flushing, heat intolerance, hair and nail changes

Question 12

hyperthyroidism cardiovascular effects

Answer 12

increased cardio output, decreased peripheral resistance, tachycardia at rest

Question 13

hyperthyroidism pulmonary effects

Answer 13

dyspnea & reduced vital capacity

Question 14

what is found in 95% of grave’s pts

Answer 14

thyroid antibodies, IgG

Question 15

clinical s&s of thyrotoxic crisis

Answer 15

Hyperthermia; tachycardia, especially atrial tachydysrhythmias; high-output heart failure; agitation or delirium; and nausea, vomiting, or diarrhea

Question 16

primary hypothyroidism types

Answer 16

Iodine deficiency
Autoimmune thyroiditis (Hashimoto disease)
Subacute thyroiditis
Painless thyroiditis
Iatrogenic thyroiditis
Postpartum thyroiditis

Question 17

hypothyroidism clinical manifestations

Answer 17

Low basal metabolic rate, cold intolerance, lethargy, tiredness, and slightly lowered basal body temperature; also possible diastolic hypertension
Myxedema

Question 18

all hormones released from the adrenal cortex are synthesized by

Answer 18

cholesterol

Question 19

disorders of the adrenal cortex

Answer 19

cushings disease
virilization
hyperaldosteronism
addison disease

Question 20

addisons disease marked by

Answer 20

hyperpigmentation, weight loss, fatigue, low blood pressure, poor appetite

Question 21

thyrotoxicosis

Answer 21

condition caused by excessive TH

Question 22

grave’s disease

Answer 22

the most common form of hyperthyroidism; caused by an autoimmune defect that creates antibodies (95% of pt) that stimulate the overproduction of TH, causing TSH and TrH suppression

Question 23

grave’s clinical manifestation

Answer 23

exophthalmos (dt ^ hyaluronic acid)
orbital fat accumulation
diplopia
pretibial myxedema (swelling

Question 24

grave’s tx

Answer 24

rad I-
sx
doesn’t remove leg edema or eye conditions

Question 25

1º hypothyroidism

Answer 25

``` I- deficiency hashimoto's disease (autoimmune) subacute thyroiditis (nonbacterial inflammation) painless thyroiditis Iatrogenic thyroiditis postpartum thyroiditis ```

Question 26

congenital hypothyroidism

Answer 26

TH deficiency at birth, can cause cretinism if not tx neonatal screening T4 for tx

Question 27

thyroid carcinoma

Answer 27

most common thyroid malignancy from rad ∆ in voice and swallowing dyspnea dt tumor growth may have normal T3/T4 lvls

Question 28

myxedema

Answer 28

non-pitting, boggy edema of the skin in hypothyroidism, esp around eyes, hands, feet, tongue

Question 29

adrenal hyperfunction cm

Answer 29

``` dt hypercortisolism wt gain glucose intolerance muscle wasting/weakness v bone density easily damaged skin vasoconstriction/HTN i.s suppression neuro ∆ ```

Question 30

adrenal hyperfunction dx

Answer 30

urinary free cortisol < 100 ug/day pit MRI inf petrosal sinus sample

Question 31

cushing's disease

Answer 31

excessive ACTH secretion most common in 30-50 women most have pit microadenoma w hypercortisolism

Question 32

addison's disease cm

Answer 32

``` hypocortisolism, hypoaldosteronism weakness, fatigue hyperpigmentation wt loss, poor appetite hypoTN ```

Question 33

2º hypocortisolism

Answer 33

addisonian crisis prolonged admin of exogenous glucocorticoids (pred) inhibits ACTH secretion CM: similar to Addison's, no hyperpigmentation

Question 34

DM

Answer 34

dysfunction of endocrine pancreas affects metabolism characterized by hyperglycemia

Question 35

DM dx

Answer 35

1+ NFG > 7 mmol/L 2hrPG > 11.1 mmol/L, confirmed next day 3 Ps (polydipsia/phagia/uria) HgBA1C

Question 36

hyperglycemia

Answer 36

high blood sugar, 80-90% of B-cells must be lost before it occurs, alongside abnormal glucagon

Question 37

type 1 DM

Answer 37

IDDM unknown cause, rt genetic and environment can be immune/non-immune

Question 38

non-immune T1DM

Answer 38

occurs 2º to other diseases (ex pancreatitis)

Question 39

immune t1dm

Answer 39

cell-mediated destruction of B-cells, w antibodies found in 85-90% HLA-DR4 strongly associated

Question 40

4 characteristics of t1dm

Answer 40

genetic susceptibility long preclinical period immunologically mediated destruction of B-cells hyperglycemia

Question 41

t1dm clinical manifestations

Answer 41

3 Ps wt loss fatigue dradual insulin deficiency and hyperglycemia

Question 42

t1dm tx

Answer 42

``` insulin meal planning exercise self-monitoring transplant (temporary) ```

Question 43

ketoacidosis

Answer 43

excessive production of ketones, making the blood acid, body compensates by blowing off acetone, giving breath a fruity scent diabetic coma may be 1st manifestation

Question 44

t2dm

Answer 44

more common than T1 genetic and environmental interaction, obesity and sedentary major factor is insulin resist

Question 45

t2dm patho

Answer 45

gradual ^ in insulin resist dt lifestyle factors, many years of hyperinsulinemia, eventually B-cell responsiveness drops, hypoglycemia occurs

Question 46

t2dm cm

Answer 46

often nonspecific, over 30 oft overwt, dyslipidemic, hyperinsulinemic, HTN PCOS x7 risk onset 7+ yrs before dx

Question 47

t2dm tx

Answer 47

restoration of euglycemia wt loss, exercise insulin, antihyperglycemics

Question 48

hypoglycemia

Answer 48

low blood sugar (<3.5 mmol/L) oft when tx w insulin (insulin shock) dt hypothalamus sensing low glucose

Question 49

hypoglycemia cm

Answer 49

tachycardia, palpitations diaphoresis, pallor tremors, anxiety coma, death

Question 50

hypoglycemia tx

Answer 50

glucagon/glucose

Question 51

dka

Answer 51

absolute deficiency of insulin and ^ in insulin counterregulatory H common fx incl: illness, interruption of insulin tx most common in IDDM

Question 52

dka patho

Answer 52

increased production of glucose ketones for fuel hyperketonemia dt peripheral ketone impairment cir of strong acids w/out bicarb buffer metabolic acidosis

Question 53

dka cm

Answer 53

``` kussmaul resp postural hypoTN CNS depression Anorexia Nausea, abd pain polyuria, thirst glucosuria, ketonuria ```

Question 54

dka dx

Answer 54

serum glucose > 250 mg/dL serum bicarb < 18 mg/dL pH < 7.3 anion gap

Question 55

dka tx

Answer 55

serum glucose > 250 mg/dL serum bicarb < 18 mg/dL pH < 7.3 anion gap

Question 56

HHNS

Answer 56

hyperosmolar hyperglycemic nonketotic syndrome life threatening, in NIDDM dt infection, rx, nonadherence, coexisting disease

Question 57

hhns patho

Answer 57

far more fluid deficiency in HHNS | higher glucose and glucose in HHNS

Question 58

hhns cm

Answer 58

``` Glycosuria, polyuria dehydration neuro ∆ glucose > 600 mg/dL absent/low urine ketones ```

Question 59

diabetic neuropathy

Answer 59

nerve damage that occurs because of the metabolic derangements associated with DM

Question 60

diabetic retinopathy

Answer 60

retinal ischemia dt bv ∆ and RBC aggregation

Question 61

diabetic nephropathy

Answer 61

Most common cause of ESRD | damage to glomeruli dt ^ P and glucose lvls

Question 62

diabetic cad and pvd

Answer 62

Most common cause of ESRD | damage to glomeruli dt ^ P and glucose lvls

Question 63

diabetic infection risk

Answer 63

``` impaired senses hypoxemia/low bld supply suppressed i.s and delayed healing rapid pathogen replication dt ^ glucose hypoxia glycosylated HgB impaires O2 release ```