Cps Spring Exam 3: Dermatology/endocrine

Front 1

how would you interpret/treat:

before breakfast = 210
before bed = 110
3 am fasting = 110

Back 1

the is the DAWN phenomenon
it is secondary to increased GH release between 5-8 am that antagonizes insulin thus causing the early AM HYPERglycemia.
Treatment is to divide the NPH dose between dinner and bedtime or change to a basal insulin

Front 2

treat/interpret:
before lunch = 200

Back 2

too large of a breakfast meal or increase the dose of reg or RA insulin at breakfast

Front 3

interpret/treat
before dinner = 220

Back 3

considering diet, possibly too large a meal at lunch or increase dose of NPH at breakfast or reg or RA at lunch

Front 4

T/F
Diabetes mellitus, diabetes insipidus, and psychogenic polydipsia are associated with polyuria.
DM: osmotic diuresis is the cause
DI and psychogenic polydipsia: the loss of free water is the cause

Back 4

True

Front 5

T/F
Dysmenorrhea is most commonly due to endometriosis.

Back 5

False
it is most commonly caused by increased PGF2, which increases uterine smooth muscle contractions. Endometriosis is the most common cause of secondary dysmenorrhea

Front 6

T/F
There may be cross-reactivity of bovine serum albumin derived from drinking cows milk with antigens in the b-cells. hence antibodies against BSA may also destroy b-cell.

Back 6

True

Front 7

T/F
Blurry vision in patients who first present with DM is most commonly due to retinopathy

Back 7

False
glucose is converted to sorbitol in the lens alters the refractive index and causes blurry vision
later on retinopathy may cause blurry vision

Front 8

T/F
Urine dipsticks for glucose are specific for glucose and no other reducing substances.

Back 8

True

Front 9

T/F
Urine dipsticks for ketones detect acetone, acetoacetate, and b-OHB.

Back 9

False
Nitroprusside does NOT detect b-OHB

Front 10

T/F
B-blockers block all of the adrenergic symptoms associated with insulin-induced HYOPglycemia.

Back 10

False
they do not block sweating

Front 11

T/F
Human insulin is less likely to result in insulin resistance due to antibodies when compared to animal derived insulins.

Back 11

True

Front 12

T/F
Type II DM is more common than type I DM and has the greatest association with a positive family history

Back 12

True

Front 13

Biphasic insulin release occurs with:

Back 13

HYPERglycemia

Front 14

what controls glucose levels in the fed state?

Back 14

INSULIN

Front 15

what controls blood glucose levels in the fasting state?

Back 15

Glucagon via its glycogenolytic properties and ultimately its gluconeogenic properties maintains the blood glucose

Front 16

where is Preproinsulin synthesized?

Back 16

in the rough endoplasmic reticulum of the beta cells in the pancreatic islets and is cleaved to form proinsulin

Front 17

where does the cleavage of C Peptide occur in order to yield insulin?

Back 17

Golgi apparatus

Front 18

what is the best marker for endogenous insulin release?

Back 18

C Peptide

Front 19

T/F
Insulin normally has a biphasic release

Back 19

True

Front 20

describe the biphasic release of insulin

Back 20

there is first and immediate release of insulin from stored levels followed by a protracted release from the synthesis of new insulin

Front 21

T/F
the immediate release of insulin is impaired in early diabetes.

Back 21

True

Front 22

how is the defect of insulin release in early diabetes detected?

Back 22

the defect is detected by infusing glucose and collecting insulin levels minutes apart and noting the impaired response

Front 23

what is the only stimuli for insulin release that stimulates both phases?

Back 23

HYPERglycemia stimulates both phases of insulin release

Front 24

what are the stimuli for insulin release that just stimulate the immediate release?

Back 24

GIP released once the gastric meal hits the duodenum
aminogenic stimulation by leucine and arginine
caffeine
sulfonylurea compounds
hyperkalemia
other hormones like gastrin, secretin, cholecystokinin

Front 25

what factors impair insulin release?

Back 25

HYPOkalmeia and counteraction of many hormones: like gastrin, glucagon, GH, adrenocorticotrophic hormone, cortisol, catecholamines, somatostatin, and thyroxine.

Front 26

describe the binding of insulin.

Back 26

insulin binds to receptor sites on the membrane of the adipose and muslce
It activates tyrosine specific kinase, which:
1. activates protein synthesis
2. activates DNA synthesis
3. activates/inactivates enzymes in the mT

Front 27

what does insulin cause to happen to GLUT receptors?

Back 27

translocation of GLUT from the Golgi apparatus to the plasma membrane to facilitate the uptake of glucose

Front 28

where is GLUT 2 found?

Back 28

insulin independent tissues like the liver and beta cells of islets

Front 29

where is GLUT 4 found?

Back 29

insulin dependent tissues like muscle and adipose

Front 30

T/F
the number of insulin receptors in inversely proportional to the number of adipose cells

Back 30

true
obese individuals have less receptors and are slightly glucose intolerant

Front 31

what is hyperglycemia in DKA primarily the result of?

Back 31

increased gluconeogenesis in the liver

Front 32

what is the fuel for gluconeogenesis in DKA?

Back 32

amino acids that would normally be taken up by the muscle but since insulin is not present alanine is converted to pyruvate which is a key substrate for gluconeogenesis

Front 33

what are the fatty acids from DKA utilized for?

Back 33

ketogenesis in the liver

Front 34

what are two other key sources of glucose in DKA?

Back 34

1. glucose that would have be utilized by the adipose and muscle in the presence of insulin
2. glycogenolysis due to the presence of glucagon and epinephrine

Front 35

what enhances glycogenolysis in the muscle?

Back 35

epinephrine

Front 36

what type of renal signs are caused by the hyperglycemia seen in DKA?

Back 36

hyperglycemia in DKA results in glucouria when the renal threshold is saturated. This produces osmotic diuresis with subsequent loss of hypotonic fluid including sodium, potassium, phosphate, and water

Front 37

In DKA, glycerol is the primarily used for?

Back 37

a substrate for gluconeogenesis

Front 38

what is glycerol used for in the presence of insulin?

Back 38

substrate for triacylglycerol synthesis

Front 39

T/F
in DKA you would expect an increase in the beta oxidation of fatty acids

Back 39

True
there is an increase in beta oxidation of fatty acids, since malonyl coA, the inhibitor of carnitine acyltransferase is not present. Recall that insulin enhanced fatty acid synthesis is responsible for production of malonyl CoA, therefor in the absence of insulin not only reduces fatty acid synthesis, but also increases beta-oxidation of fatty acids in the mT.
One of the end products of the beta oxidation of fatty acids is acetyl CoA which is used for a substrate in ketogenesis

Front 40

T/F
in DKA you would expect a decrease in glycolysis

Back 40

True
in the absence of insulin and the presence of glucagon

Front 41

T/F
in DKA there is a decreased activation of capillary lipoprotein lipase

Back 41

true
since insulin, which is responsible for its synthesis is absent. This results in a build up of chylomicrons, and very low density lipoproteins and potential for severe hyperlipidemia
Eruptive xanthomas and acute pancreatitis are two potential complications of hyperlipidemia

Front 42

T/F
in DKA there is a decrease in the breakdown of chylomicrons and VLDL.

Back 42

True
capillary lipoprotein lipase is decreased

Front 43

T/F
in DKA there is an increased activation of hormone sensitive lipase in the adipose by glucagon and epinephrine

Back 43

True
this increases the release of fatty acids and glycerol, the former (glucagon) used in ketogenesis and the later (epinephrine) a substrate for gluconeogenesis

Front 44

ketone bodies in DKA derive from acetyl cOA which is primarily derived from?

Back 44

the beta oxidation of fatty acids

Front 45

T/F
DKA is primarily seen in Type II diabetics

Back 45

False
DKA is primarily seen in Type I DM because there is no insulin produced

Front 46

T/F
there is enough insulin produced in type II DM to prevent DKA, but not enough to prevent HYPERglycemia

Back 46

True

Front 47

is there an increase in beta oxidation of fatty acids in DKA?

Back 47

yes, there is an increase in beta oxidation of fatty acids in DKA, since malonyl CoA, the inhibitor of carnitine acyltransferase is not present. Recall, that insulin enhanced fatty acid synthesis is responsible for the production of malonyl CoA therefore the absence of insulin not only reduces fatty acid synthesis, but also increases the beta oxidation of fatty acids in the mT.
One of the end products of beta oxidation of fatty acids is acetyl CoA which is used as a substrate for ketogenesis, which primarily occurs in the liver.

Front 48

what is the reaction for acetyl CoA > BHB?

Back 48

Acetyl CoA > acetoaceto CoA > HMG CoA > AcAc > BHB

Front 49

what is responsible for the fruity odor to the breath of a person in DKA?

Back 49

AcAc breaks down into acetone

Front 50

what results in an increased AG metabolic acidosis in DKA?

Back 50

increased AcAc and BHB

Front 51

patient presents with panhypopituitarism, what are total serum T4 and TSH?

Back 51

decreased total serum T4
decreased TSH

Front 52

woman is taking OCPs, what would her total serum T4 and TSH be?

Back 52

Increased Total Serum T4
Normal Serum TSH
- increased TBG because of the OCPs

Front 53

Patient with normal thyroid exam who has nephrotic syndrome. what do their thyroid studies look like?

Back 53

Decreased Total Serum T4
Normal Serum TSH
- loss of TBG in the urine

Front 54

Patient has primary hypothyroidism. what do their thyroid studies look like?

Back 54

decreased total T4
increased TSH

Front 55

Overweight patient with sinus tachycardia, systolic HTN, fine tremor. Thyroid gland not palpable. She says she is taking a "diet pill"
Thyroid studies?

Back 55

Decreased TSH
Increased Serum Total T4
- woman is taking excess thyroid hormone to lose weight

Front 56

T/F
T/F
The combination of Hashimoto's thyroiditis and pernicious anemia has no causal relationship.

Back 56

False
they are both autoimmune diseases, hence they may occur together

Front 57

T/F
Antibodies against HCV indicate immunity to future exposure to the virus

Back 57

False
they indicate active disease
no protective antibodies have been identified to date

Front 58

T/F
Yellow skin with white sclera is due to accumulation of retinoic acid in the skin

Back 58

False
b-carotenes are normally converted to retinoic acid in the intestine with the aid of thyroxine, hence hypothyroidism leads to an accumulation of b-carotenes not retinoic acid

Front 59

T/F
b-carotenemia may cause vitamin A toxicity

Back 59

Fasle
only an increase in retinoic acid can produce toxicity

Front 60

T/F
an elevated serum CK in primary hypothyroidism is secondary to proximal muscle myopathy

Back 60

True

Front 61

T/F
Hypercholesterolemia in primary hypohthyroidism is secondary to reduced synthesis of LDL receptors

Back 61

True

Front 62

T/F
Puffiness around the eyes in primary hypothyroidism is due to an increase in mucopolysaccharide deposition.

Back 62

True

Front 63

T/F
Tinel's sign and Phalen's sign are used to diagnose median nerve entrapment.

Back 63

True
Tinel's sign" involves tapping over the median nerve
Phalen's sign: compression of the nerve

Front 64

T/F
A schilling's test could still be performed on this patient even though they are taking B12. it would show reabsorption of radioactive B12 after administration of both IF and radioactive B12

Back 64

true

Front 65

T/F
HCV is the most common infection transmitted by blood transfusion.

Back 65

False
CMV is the most common

Front 66

T/F
HCV is the most common cause of post transfusion hepatitis

Back 66

True

Front 67

T/F
Corticosteroids are essential in the treatment of chronic HCV

Back 67

False
corticosteroids are contraindicated in HCV
a-INF is the treatment of choice

Front 68

T/F
Graves disease and Hashimoto's thyroiditis have thyroid stimulating immunoglobulins however they are stimulatory in Graves disease and inhibitory in Hashimoto's thyroiditis.

Back 68

True

Front 69

T/F
total serum T4 levels are best used to follow patients being treated for hypothyroidism with levothyroxine.

Back 69

False
TSH is the best test and combined with free T4

Front 70

what are the diagnostic criteria for DM?

Back 70

1. FBS > 126 mg/dL
2. 2 hr. PG > 200 mg/dL during oral glucose test
3. Random glucose > 200 mg/dL with symptoms or hyperglycemic crisis
4. HbA1c > 6.5%

Front 71

what are the diagnostic criteria for Impaired Glucose tolerance?

Back 71

1. FBS > 100 and < 126 mg/dL
2. 2 hr. PG > 140 and < 200 mg/dL
3. HbA1c 5.7-6.4%

Front 72

describe the pathogenesis behind TYPE I DM?

Back 72

- absence of insulin secretion
- autoimmune/idiopathic
- rapid onset of symptoms
- insulin tx required to sustain life
- HLA association
- younger/thin patients

Front 73

describe the pathogenesis behind TYPE II DM.

Back 73

- reduced insulin secretion or raised insulin
- NO HLA/autoimmune association
- Insideous onset of symptoms
- insulin tx not required to sustain life except in patients who fail OAD tx
- older/obese patients

Front 74

which type of diabetes is ketoacidosis associated with?

Back 74

type I DM
- they have NO insulin

Front 75

if your patient has NO C-peptide, what is that a diagnosis for?

Back 75

Type I DM

Front 76

what are frequent symptoms of Type II DM?

Back 76

3 P's:
polyuria
polydipsia
polyphagia

Front 77

what are the acute complications of Diabetes?

Back 77

1. HYPOglycemia (type I & 2)
- blood sugar < 50 mg/dL
2. DKA (type I)
-absolute insulin deficiency with production of large amount of ketones
3. HYPERglycemia hyperosmolar state (type II DM)
- marked elevation of blood sugar with severe dehydration

Front 78

what are the chronic complications of Diabetes?

Back 78

Macrovascular:
1. heart attack
2. stroke
3. Peripheral vascular disease
Microvascular
1. eye disease leading to blindess
2. kidney disease leading to kidney failure
3. neuropathy

Front 79

what are the guideline/goals in prevention of complications of DM?

Back 79

1. HbA1c < 7.0%
2. LDL < 100 mg/dL (< 70 mg/dL in CVD hx)
3. BP < 130/80 mmHg

Front 80

describe what the HbA1C is.

Back 80

Glycosylated hemoglobin
- irreversible binding of glucose with amino acids on the globulin component of Hb
- accurate average level of BG for last 8-12 weeks
- use as monitor to measure level of control of BG
- Normal < 5.7%

Front 81

how are Biguanides used in the treatment of Type II DM?

Back 81

decrease hepatic glucose production and increase insulin mediated peripheral glucose uptake
efficacy: decrease fasting plasma glucose 60-80 mg/dL
reduce A1c: 1.5-2.0 %

Front 82

what drugs are in the Biguanides class of diabetic medication?

Back 82

Metformin

Front 83

who is Metformin contraindicated in?

Back 83

patients with impaired renal function
NO Biguanides

Front 84

GLP-1 receptor analogues, Victoza, indicated in what disease?

Back 84

Type II DM as an adjunct to diet and exercise
once daily SC administration

Front 85

what are the adverse drug reactions of GLP-1 analogues, Victoza?

Back 85

nausea, vomiting, diarrhea, weight loss

Front 86

when is Victoza, GLP-1 analogue, contraindicated?

Back 86

h/o medullary thyroid cancer

Front 87

what is considered to be one of the 5 highest risk medicines in the inpatient setting?

Back 87

Insulin therapy

Front 88

what are the rapid acting insulins?

Back 88

Lispro
Aspart
Glulisine

Front 89

what are the short acting insulins?

Back 89

Regular human insulin

Front 90

what are the intermediate acting insulins?

Back 90

Human NPH

Front 91

what are the long acting insulins?

Back 91

Detemir
Glargine

Front 92

how do you initiate insulin therapy?

Back 92

Empiric dosing (daily dose)
- Insulin analogues
> Type 1: 0.5 u/kg/d
> Type 2: 0.7-1.0 u/kg/d (obesity & exercise)
- Give 50% Basal insulin
- Give 50% Bolus insulin
Split into 3 doses
Adjust accordingly > carb counting

Front 93

why is insulin given at a higher dose to type II DM patients when initiating insulin therapy?

Back 93

Type II doses are higher because there is an insulin resistance present.