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Flashcards in endo DIT Deck (234):
1

cAMP modifying hormones (11)

FSH
LH
TSH
hCG
ACTH
MSH
GHRH
PTH
Calcitonin
glucagon
V2 vassopressin

2

IP3 modifying hormones(4)

GNRH
TRH
Oxytocin
vasopressin (v1)

3

Tyrosine kinase receptor modulators

GH
Insulin
insulin like growth factor
Platelet derived growth factor
fibroblast growth factor
Cytokines
prolactin

4

cGMP modulators (2)

NO
ANP

the vasodialators

5

Preganancy leads to an increase of what liver product that may affect hormone affects

binding globulin decreasing the amount of free active hormone

Thyroid - TGH for example

6

Steroid receptor modulated hormone (5)

estrogen, progesteron, testosterone
glucocorticoids
aldosterone
Thyroid hormone
Vit D

7

Availabilty of binding hormone affects 2 things

amount of free hormone
activity of steroid hormone

8

increased sex binding hormone may have what affect on men?

gynectomastia due to decreased free testosterone

9

decreased sex binding hormone in women may have what effect in women?

hurtusism

10

ACTH and MSH are synthesized by what precursor?

Clinical relevance?

POMC

Leads to hyperpigmentation w/ primary adrenal insufficency

11

Hyperprolactenima due to? (4)

pregnancy/ nipple stim
stress
prolactinoma
dopamine antagonists ) haloperidol, risperidone, domperidone, metoclopramide, methydopa

12

Symptoms of hyperprolactinemia in

pre meno women

post meno?

Men

hypogonadism -> infertility, oligo/amennorhea, rarely galatorrhea

post meno - asymptomatic, maybe galactorrea

Men - (low testosterone)low labido, impotence, infertility, gynectomastia, rarely galactorrhea

remember, prolactin inhibits FSH and LH

13

Clinical uses of octreotide(3)

pituitary excess
-acromegaly, thyrotropinoma, ACTH secreting hormones

GI endocrine excess
-Zollinger ellison syndrome, carcinoid, VIPoma, glucagona, insulinoma

Need to reduce splanchnic circulation
-portal HTN, bleeding peptic ulcers

14

infertility, galactorrhea and bitemporal hemanopsia

prolactinoma

15

inability to breastfeed, amenorrhea, cold intolerance

sheehan syndrome

16

Which hormones share a common alpha subunit(4)

TSH
LH
FSH
b hCG

17

anterior pituitary is derived from

rathke's pouch
surface ectoderm

18

posterior pituitary is derived from

neuroectoderm

19

ADH is stimulated w/ ?(3)

Decreased w?(3)

nicotine
opiates
high serum osmolarity
low volume contraction

ethanol
atrial naturetic factor
low serum osmolarity

20

Oxytocin important w/

stimulated w?

pregnancy and breast feeding
uterine contraction ( return to normal size/clamp bleeding)
milk ejection

cervical dilation
inhibited w/ alcohol and stress

21

inhibit feeds back and blocks

FSH

22

progesterone and testosterone feedback on

LH

23

ACTH is stimulated to release w/(2)

Stress
CRH from the hypothalamus

24

TSH is released from?

inhibited by?

Stimulated by?

TSH from the pituitary

inhibited by T3 and T4 levels

Stimulated by TRH from hypothalamus

25

Prolactin leads to inhibition of ?

Prolactin stimulated by?

ovulation via blocking of LH and FSH
- stimulates milk production and breast development

stimulated to release by TRH and less Dopamine inhibition

26

GH effects (4)

increases growth
decreases glucose uptake (insulin resistent- mobilize gluc)
increase protein synth
increase organ size and lean body mass

27

upstream control of GH (2)

other regulators of release(environmental)

GHRH - releases
GHIH (somatostatin)

+: exercise, sleep, hypoglycemia, puberty, estrogen, stress, endogenous opiods

-: obesity, hyperglycemia, pregnancy

28

Downstream response to increase of GH

increase of IGF 1

29

Rx for prolactinoma

dopamine agonists
- bromocriptine
-cabergoline

30

Presentation of Acromegaly

large tounge
deep voice
large hands/feet
coarse facial feature
impaired glucose tolerance

31

Diagnosis of acromegaly (2)

measure IGF1 - more stable vs pulsitile GH

failure of suppression of GH from the pituitary adenoma w/ glucose given

32

Zona glomerulosa secretes

responds to

Aldosterone

renin

33

Zona fasiculata secretes?

responds to

cortisol

ACTH and CRH

34

Zona reticularis secretes?

Responds to?

androgens

ACTH and CRH

35

Adrenal tumor in adult vs kids

One key difference

Pheochromocytoma in adults -> episodic periods of hypertension

Neuroblastoma in kids -> maybe chronic HTN.

36

Symptoms of a pheochromocytoma (4)

HA, Sweats, Tachy, Eposodic HTN

37

Fetal adrenal gland is important in

secretion of cortisol for fetal lung maturation

responds to CRH and ACTH

38

ketoconazole acts to block what enzyme?

desmolase
-conversion of cholesterol -> pregnenolone

39

ACTH acts on what enzyme to encourage hormone synthesis?

Desmolase

40

Angitension II acts on adrenal steroid synthesis by increasing the action of what enzyme

aldoserone synthase

41

One thing in common w/ adrenal hyperplasia

all have decrease production of cortisol
-> ACTH ramps up
-> stimualtes adrenal cortex
-> adrenal hyperplasia

42

Enzyme responsible for converting testosterone to a more active enzyme

Blocked by what drug

5 alpha reductase

blocked by finasteride

43

estone, estradiol and estriol all need what enzyme to be made?

Aromatase

44

Features of 3 beta hydroxysteriod deficiency? (3)

Inability to produce
-glucocorticoids
-mineralcorticoids
-androstenedione-> testosterone or estrone
-estrogens

Excessive Na excretion in the urine (salt wasting)

Early death

45

What features are characteristic in 17 alpha hydroxylase deficiency

inability to produce androgens/sex hormones and cortisol
-> phenotypic female that is unable to mature (no androstendione)

Hypertension w/ everything being shunted to aldosterone production
-Na and water retention

46

Desmolase is responsible for what

converting cholesterol to pregnenolone starting the adrenal steroid pathway

rate limiter

47

What features are characteristic of a deficiency in 21 alpha hydroxylase? (3)

Can't make cortisol or aldosterone ->

Increased ACTH

Hypotension and salt wasting w/ou Aldosterone

Masculinization w/ everything shunted to the right (androstenedione)

48

What features are characteristic of 11 beta hydroxylase deficiency?

Inability to produce Aldosterone and Cortisol

Increased ACTH

Increased production of 11 deoxycorticosterone
-Acts as a weak aldosterone -> HTN

masculinization with a shift to sex hormone production (androstenedione)

49

2 deficiencies characteristic in hypertension

11 beta hydroxylase
17 alpha hydroxylase

50

2 deficiencies characteristic in masculinization

21 hydroxylase
11 beta hydroxylase

51

deficiency characteristic in hypotension

masculinization of feminization

21 hydroxylase

masculinization

52

Cortisol maintains BP how?

increasing alpha 1 receptors on the vasculature increasing sensitivity

53

Cortisol functions/effects on the body (5)

BBIG

Maintain BP increasing alpha receptors on vasculature

Decreases bone formation

Anti inflam/immune suppresive
-neutropenia w/ adhesion disruption, inhibits prostaglandin production, block IL2

Insulin resistance (diabetogenic)

Gluconeogenesis/lipolysis and proteolysis ( increases enzyme expression)-> mobilizes sugars

54

Why is there a rise in WBC after giving a glucocorticoid

neutropenia transient due to mobilization of WBC stores in the vasculature

55

Regulation of cortisol 3 steps

CRH from the hypothalamus

-> Pituitary releasing ACTH

-> ACTH acts on the adrenal cortex (desmolase) to increase production of cortisol in the zona fasiculata

56

What can induce prolonged secretion of cortisol

chronic stress

57

Symptoms of Cushing Syndrome

BAM CUSHINGOID

Buffalo hump
Amenorrhea
Moon Fascies

Crazy
Ulcers (peptic)
Skin ∆s (striae, acne)
HTN
Infection
Necrosis of femoral head
glaucoma.cataracts
Osteroperosis
Immunosuppression
DM

58

4 Causes of Cushing Syndrome

Iatrogenic (exogenous steriods - #1)
Pituitary Adenoma - Cushings disease (ACTH)
Ectopic ACTH production - small cell
Adrenal adenoma (primary high cortisol)

59

Dexamethasone suppression test w/ high dose will suppress cortisol of which cause of cushing syndrome?

Suppreses pituitary adenoma

ACTH levels to differentiate between adrenal adenoma and small cell - both unsuppresed
-high ACTH in ectopic (small cell)
-low ACTH in adrenal adenoma

60

Presentation of HTN, hypokalemia and metabolic alkalosis due to

Conn Syndrome
- Primary hyperaldosteronism

Have a low renin level

61

primary hyperaldosteronism name?

Triad of symptoms

Conn syndrome

See:
- Hypertension
-Hypokalemia
- metabolic alkalosis

62

Rx for Conn syndrome (2)

epleronone and spironolactone

Surgery

prevent hyperaldosertone

63

Secondary hyperaldosteronism due to: (4)

renal artery stenosis

chronic renal failure

CHF

hypo protein states (edema perceived fluid loss)
-cirrosis
-nephrotic syndrome

Going to have high renin levels (appropriately)

64

Fludrocortizone

highly active synthetic mineral corticoid

65

Stimulation of Aldosterone

decreased aldosterone secretion

Decreased
-high Na

Increased in
- low Na or volume
-Hyperkalemia

66

Addisons is most commonly due to

Presentation

autoimmune attack of the adrenal cortex -> chronic primary adrenal insufficiency ( less aldosterone, cortisol)
--Less commonly: TB and METs

low aldosterone and cortisol ->
-hypotension
-skin pigmentation
-hyperkalemia
- acidosis

-malaise
-anorexia
-fatigue
- weight loss

67

Primary adrenal insufficiency can be distinguished from secondary adrenal insufficiency by :

Increased amount of ACTH in primary adrenal insufficiency

Decreased in secondary adrenal insufficiency (problem is in the pituitary

68

Secondary adrenal insufficiency presents as?

Due to

less ACTH due disruption of the pituitary ->


malaise
fatigue
weight loss
anorexia

NO skin pigmentation (no POMC)
NO hyperkalemia/hypotension (Aldosterone from renin)

69

How do you have hypotension w/ Addison's

chronic primary adrenal insufficiency

no alpha 1 upregulation w/ cortisol
No aldosterone leading to water and Na retention

70

Cause of acute adrenal insufficiency

adrenal hemorrhage w/ Nessieria meningitidia
(waterhouse frederichsen syndrome

- Septic
- DIC
endotoxic shock

71

Urine product detecting pheo?

Serum product looking for a pheo?

VMA ( vanilla mandelin acid) in urine

Normetanephrine and metanephrine in serum

catecholamine breakdown products

72

Pheos can be associated w which 3 tumor syndromes

MEN 2A
MEN 2B
neurofibromatosis 1

73

Erythropoeitin can be secreted in 4 tumors

Pheochromocytoma
Renal cell carcinoma
hemangioblastoma
hepatocellular carcinoma

74

Medical treatment for a pheochromocytoma?(3 steps

1st manage the BP w/ alpha 1 antagonist - phenoxybenzamine

2. maybe give a beta blocker

3. surgically remove the chromatin cell/adrenal medulla cancer

75

Rule of 10s w/ a pheochromocytoma (5)

90% benign
90% adults
90% adrenal - occasionally extra renal
90% do not calcify
90% unilateral

76

most common tumor of the adrenal medulla in kids

presentation/location?

test for urine?

neuroblastoma

tumor can be anywhere in the sympathetic chain 40% adrenal

less likely episodic HTN


homovanillic acid (dopamine breakdown) in urine

77

neuroblastoma is associated w. over expression of this oncgene

Histological stain to help differentiate

n-myc

can stain for neurofilaments

78

Bombeison tumor marker associated w?

neuroblastoma

79

MEN 1 tumors

associated mutation

mutation in p53

3 Ps

Pituitary adenoma
Parathyroid adenoma**
Pancreatic tumors (VIPoma, gastrinoma, insulinoma, zollinger ellison, glucagonomas)

80

MEN 2a tumors

associated mutation

mutation in ret gene

PP's and M

Medullary thyroid carcinoma* (secretes calcitonin)
Pheochromocytoma
Parathyroroid tumor

81

MEN 2 B tumors

associated mutation

mutation in ret gene

1P and 2 Ms

Medullary Thyroid Carcinoma
Pheochromocytoma
Mucosal neuromas (ganlioneuromatosis of the Gi and oral cavity)

82

MEN syndrome inheritence

all auto recessive

83

presentation of kidney stones or stomach ulcers w/ weigh loss

be concerned of what?

MEN 1
-parathyroid tumor -> PTH -> excess Ca
-Pancreatic tumor -> gastrinoma

84

most common cause of Conn syndrome

adrenal hyperplasia

85

Thyroid is derived from what tissue in what location?

ectoderm
originates from the floor of the primitive and descends into the neck via the thyroglossal duct

foramen cecum is site of origination and most common site of ectopic thyroid tissue

86

anterior midline mass that moves with swallowing is what?

Derived from

thyroglossal duct cyst that is due to persistent thyroglossal duct

87

Function of T3 and T4

ramps up metabolism
- bone growth (synergy w/ GH)
-CNS maturation
increase in beta 1 receptors of the heart
increased basal metabolic rate via increased Na/K atpase activity
increased glycogenolysis, gluconeogenesis. lipolysis

88

Thyroxine binding globulin increased w?

Decreased w?

resulting lab values

Increased TBG in pregnancy and OCP use
- leads to increase in total T4 and T3 w/ binding of free hormone
-percieved depletion of free hormone leads to increase in release which is again bound up -> normal/elevated T3/T4

TSH can be low due to similarity to beta hCG

89

Enzyme responsible for oxidation and organification go iodide?

Peroxidase

90

Iodide is brought into the follicular cell via?

Bound to what AA residue

Na/I cotransporter
then oxidized to Iodine and bound tyrosine AA residue on thyroglobulin (organification)

91

2 drugs to prevent thyroid hormone synthesis

Which is preferred overall?

Which is preferred in pregnancy

propylthirouracil
- blocks peripheral conversion of T4-> T3
-used in 1st trimester
-generally worse SFx profile w/ agranulocytosis, liver dysfunction

methimazole
- preferred over all
- used in 2nd and 3rd trimester only due to risk aplastic cutis in 1st

92

Symptoms of hyperthyroidism

heat intolerance -> due to production/metabolism
weight loss
hyperactivity
diarrhea
increased reflexes
pretibibial myxedema - graves
warm moist skin
tachycardia

93

Lab value used to screen for hyperthyroidism

TSH would be low
-very responsive to small changes in T3 and T4

94

brief episode of hyperthyroidism followed hypothyroidism, painful thyroid on palpitation?

entire episode was preceded by what event?

subacute thryroiditis

Usually preceded by a viral/ flue like illness

95

Rx for subacute thyroiditis?

see on histology?

NSAIDs for pain for it is usually self limiting

granulomatous inflammation

96

HLA B35 assoicated w/ this thyroid pathology

see on histology

subacute thyroiditis

granulomatous inflammation

97

Focal patches of hyper functioning follicular cells working independently of TSH due to mutation in TSH receptor

Reassurance on radioactive iodide uptake?

toxic multinodular goiter

increase release of T3 and T4 seen

Look for HOT nodules -> rarely malignant

98

Jod Basedow phenomenon

patients beocmes thyrotoxicosis after being given exogenous iodine (post CT w/ contrast or amiodarone) and patient has a thyroid deficiency goiter and goes crazy w/ now iodine

99

Graves disease presents as?

Due to

presents w/ hyperthyroidism, pretibial myxedema and exothalamos due to presence of TSH receptor location; and a diffuse goiter

due to autoimmune creation of thyroid STIMULATING (odd) immunoglobins (IgG) that act as TSH -> increase of T3 and T4 release

100

HLA DR3 and HLA B* are associated w/ what thyroid pathology

Graves

101

Thyroid storm is due to?

Rx?

stress induced catecholamine surge leading to death by arrhythmia ( restless, fever, sweating, tachy, tremor, delirium, vomiting, change in mental status)

Complication of graves and other hyperthyroid disorders

Rx: beta blockers, propylthiouricil, methimazole

102

stroma ovarri teratoma

teratoma w/ functional thyroid tissue -> hyperthyroid presentation

RARE

103

recent injection using a IV contrast leads to presentation of hyperthyroidism

Jod Basedow

104

presents as hyperthyroidism post thyroidectomy or radio ablation of thyroid

given too much T3 and T4

105

graves disease TSH and T3/T4 levels

TSH is low, Thyrois stimulating immunoglobin (IgG) acting on thyroid ->

High T3/T4

106

Body mostly makes what type of thyroid hormone

T4
Stable 6-9 days. longer half life

107

histology of 3 main hypothyroid states

hashimotos
subacute thyroditis
Riedals

Hashimotos
-lymphocyte infiltration, Hurthel cells

Subacute
-granulomatous infiltration

Reidal
-fibrous w/ macrophage and eosinophil infiltration

108

Most common cause of hypothyroidism

See what in serum potentially?

hashimotos

thyroid peroxidase antibodies
antithyroglobulin antibodies

109

increase risk of what CA w/ hashimotos?

Commonly associated w?

B cell lymphoma

other autoimmune pathologies: Addisons, DM, sjogrens

110

Transient hyperthyroid for a couple months, painless thyroid, eventually hypothyroid

hashimotos

111

HLA DR5 and HLA B5 are associated w?

Hashimotos

112

Causes of congenital hypothyroidism(5)

Cretism

defect in T4 formation
developmental failure
failure of descent
iodine deficient mother (most common world wide)
transfer of mother's auto-ab/medication across placenta

113

Presentation of congenital hypothyroidism (4)

Pot bellied
mental retardation
protuberant tongue
dwarfism (lack of synergy w/GH)

114

Reidals thryroiditis presentation

thyroid replaced w/ fibrous tissue (fixed/ rock hard/ painless goiter)

concern w/ extension into local tissue and compression

Histology you see eosinophilia and macrophage infiltration

115

fixed, hard painless goiter

reidals

116

levothyroxine

synthetic T4

usually what is given once a day for hypothyroidism

117

Triiodothyronine

synthetic T3

not used as much as levothyroxine

118

Presentation of hypothyroidism

cold intolerance
weight gain
hypoactivity/lethargy
constipation
decreased reflexes
dry cool skin/brittle hair
bradycardia

119

hypothyroidism has what effect on lipid profile

increases LDL and total cholesterol

120

Papillary carcinoma prevelance and presentation (4)

most common

empty appearing nuclei/orphan annie/ ground glass
psammoma bodies
nuclear grooves
activation of tyrosine kinase receptor

121

Thyroid cancer associated w/ activation of tyrosine kinase receptor(2)

Papillary carcinoma

Medullary thyroid carcinoma

122

Risk of papillary thyroid carcinoma increases w/ (2)

smoking
childhood radiation Rx

123

Gene mutation in Ret oncogene in which thyroid carcinoma?

Also associated? (2)

Papillary thyroid carcinoma

NTRK1 mutation
BRAF gene

124

Most common mutation in the BRAF gene for thyroid carcinoma (serene/threonine kinase)

papillary

125

commonly associated thyroid cancer w/ either RAS or PAX8-PPAR mutation

follicular carcinoma

126

cancer arising from the parafollicular C cells

secretes?

Medullary thyroid cancer

Calcitonin

127

Follicular carcinoma vs adenoma

whether or not the fibrous capsule has been pierced or not

spreads hematogenousle

128

Medullary carcinoma is located where?

Associated w?(2)

parafollicular C cells
-secretes calcitonin

Associated w MEN2A and MEN 2B

129

Have a hard single fibrous nodule in an older patient be concern w?

undifferentiated/anaplastic carcinoma vs reidels in a younger patient

130

Sheets of cells in an amyloid stroma

medullary thyroid carcinoma

131

2 thyroid tumors associated w/ RET mutation

medullary carcinoma
papillary carcinoma

both tyrosine kinase activators as well

132

Thyroid tumor complications (2)

hypocalcemia due to parathyroid removal

hoarseness w/ damage of the recurrent laryngeal nerve

133

parafolliciluar cells secrete?

located?

calcitonin

located the medullary of the thyroid

Associated w/ medullary thyroid carcinoma

134

Endocrine pancreas cell types and products (3)

Glucagon from the alpha cell
insulin from the beta cell
Somatostatin from the delta cell

135

Glut 2 transporter found where(4) and responsible for

pancreatic beta cells
small intestine
liver
renal

responsible for glucose sensitivity,
insulin independent
bidirectional

136

Glut 4 transporter found where(2) and responsible for

Adipose
skeletal

Responsible for insulin sensitive take-up of glucose

137

GLUT 1 transporter found where? (2) responsible for

RBCs and the brain

responsible for insulin independent take of glucose

138

Insulin receptor is what what type

tyrosine kinase leading to increase of GLUT 4 taken in

139

How is insulin released from the beta pancreatic cell (6 steps)

increase in glucose -> Glut 2
-> aerobic glycolysis -> increase of ATP/ADP ratio
-> closing of ATP sensitive K cells
-> depolarization of cell membrane
-> opening of Voltage gated Ca channels and influx
-> vesicles containing insulin fusing and leaving

140

Results anabolic effects of insulin (4)

increase of glucose transport in skeletal muscle
increase in glycogen synthesis
increase in triglyceride synthesis
increase in protein synthesis

141

Results of glucagon catabolism(4)

glycogenolysis
gluconeogenesis
lipolysis
-> ketone body production

mobilize stored energy and eventually increases insulin secretion

142

Presentation of DM (5)

polydipsia
polyuria
polyphagia w/ weight loss (unable to get sugar in)
hyperglycemia

143

2 main pathologies of Diabetes

Nonenzymatic glycosylation
-small vessel disease: retinopathy and nephropathy
- large vessel disease: atherosclerosis, gangrene

Osmotic Damage
- neuropathy
-cataracts

144

Protective drug w/ nephropathy

ACE inhibitors

145

Nonenzymatice glycosylation in DM leads to (3)

Small vessel disease
retinopathy
- hemmorage, exudates, microneurysms(flame)

nephropathy
-nodular sclerosis (kimmerstiel wilson nodules)

Large vessel disease
-gangrene
-Atherosclerosis
-cerebrovacular disease

146

Osmotic damage in DM is due to presence of what enzyme and lack of another in what organs (4)

have in aldose reductase, glucose -> sorbitol
Deficient in sorbitol dehydrogenase

Not in Retina, lens, schwann cells, kidney

147

HLA DR3 -DQ2 and HLA DR4 DQ 8 are associated w/

DM type 1

148

Which DM has a strong hereditary predisposition?

DM type II

149

DKA is associated w/ what DM?

Type I

150

Hyperosmolar hyperglycemic state is associated w/ what DM?

Type II

151

Auto antibodies against GAD?

DM type I

152

What are some common causes of DKA?(7)

Infection- pneumonia, gastroenteritis, UTI
diabetic med reduction/omission
severe medical illness - MIC/CVA/truma
Undiagnosed DM
Dehydration
Alcohol/drug use
Corticosteriods

all mobilize stressors -> excess glucagon, catecholamine, cortiosteriods

153

Pathogenesis of DKA?

increased insulin requirements due to tstressors. body goes to plan B (gluconeogen/lipolysis etc) to get sugar into cells despite plenty of sugar around in the serum

-excess fat breakdown
-beta oxidation overwhelms w/ acetyl coA
-ketogenesis
> beta hydroxybutyrate than acetoacetate

154

Symptoms of DKA (6)

kussmaul breathing
N/V
Abdominal pain
psychosis
dehydration
fruity odor

155

Labs in DKA

H?
K?
sugars

hyperglycemia >300 mg/dL

metabolic acidosis w/ anion gap- give insulin till corrected
hyperkalemia (cells attempt to correct acidosis), polyuria -> net loss of K

156

Insulin is needed in DKA for 2 things

Lower glucose sugars
correct the metabolic acidosis prevent further ketone formation

157

Complications of DKA

murcomycosis - life threatening fungal infection
cerebral edema
cardiac arrythmia (w/ low K)-> V tach and torsades (low Mg)

158

initial treatment of DKA (3)

IV fluids
IV insulin
IV K (repleat stores)

159

why is DKA less common in Type II DM

because a little bit of insulin is available to prevent lipolysis and associated ketone generation

160

Labs in hyperosmolar hyperglycemia state?

hyperglycemia (>800)
hyperosmolar >340

in type II DM

161

mental confustion, delerium severe dehydration, N/V, ab pain, high sugars but no fruity breath

hyperosmolar hyperglycemic state

162

Why are some type II DM capable of having ketosis

hereditary predisposition to toxic production that shuts down pancreatic secretion

163

Lactic acidosis is a rare but worrisome side effect w/ this DM drug

metformin

164

DMII Drug contraindicated w/ creatine >1.5

metformin

165

Most common SFx of DMII drug is hypoglycemia

sulfonylureas

166

DMII drug that is not safe in settings of hepatic dysfunction or CHF

Glitazones/thiazolinediones

pieoglitazone
rosiglitazone

167

DMII Drugs that should not be used in patients w/ cirrhosis or inflammatory bowel disease

alpha glucosidase

Acarose
miglitol

168

DMII drugs not associated w/ weight gain (3)

metformin

GLP1 Inhibitors

DPP4 inhibitors

169

DMII drugs metabolized by the liver; excellent for patients w/ kidney disease

Thiazolidineodiones

170

DMII drugs good for weight loss

GLP 1 analogs

171

DMII medication that lowers LDL and triglercides as a bonus

metformin

172

GLP 1 analogs (2)

exenatide
liraglutide

173

sulfonureas (3)

glyburide
glimepride
glipizide

174

DPP4 inhibitors (3)

linagliptan
saxagliptan
sitagliptan

175

Metabolic syndrome 5 categories

Abdominal obesity - waist > 40 in males; >35 females
BP > 130/85
HDL < 40mg/dL male- 150 mg/dL
Fasting glucose >100

176

Meds linked to increase hunger (4)

Atypical antipsychotis
miratzapine
Several DM drugs
- insulin/TZD/ sulfonuresas
Progestins

177

Common causes of nonalcoholic steatohepatitis(4)

pathogenesis

obesity, Type II DM, hyperlipidemia, insulin resisitance

the resistance -> lipid accumulation in the liver -> inflammation and PMN infiltration

progression fatty liver disease -> steatohepatitis -> cirrosis

178

Diagnose fatty liver disease (2)

Imaging
-US
-CT
-MRI
- Magnetic resonance spectoscopy

Liver biopsy-> only those at risk for progression

179

Rx for fatty liver disease (5)

avoid alcohol
weight loss
control DM
TZDs -pioglitazone, improves LFTs and possibly histology
Metformin shows improvement

180

BMI formula

Weight in kg / (height in meters)^2

181

Hormone released by adipocytes regulating hunger

Acts where (2)

Leptin

in the hypothalamus
-inhibits Lateral nucleus
-stimulates VMN

182

5 hypothalamus nuclei imlplicated in hunger

paraventricular nuclei
arcuate nuclei
Dorsal medial nucleus -stimulates GI

Lateral area (hunger, leptin inhibits)
ventromedial area (satiety, leptin stimulates)

183

Lipodystrophy is what and could be due to ?

aplasia and distortion of the architecture of adipocytes
- ex: buffalo hump

Can be due to
- HIV medications (protease inhibitors)
- leptin deficiency

184

Causes of hypercalcemia (7)

Primary hyperparathyroidism(90%)
-solitary parathyroid adenoma (MEN1?)
-parathyroid hyperplasia (MED2a?)

Maligancy
-PTHrP (squamous cell, renal cell, breast METs to bone)
-multiple myeloma

Excess Vitamon D ingestion
milk alkali syndrome - antacid ingestion
granulomatous disease (sarcoid/TB- macrophage Vit D)
Increased bone turn over
Thiazides

185

Sympathetic cervical ganglia controls the parathyroids how?

controlling the bloodflow to the region

186

what cell secretes Calcitonin?

PTH?

calcitonin - c cells/parafollicular in the thyroid

PTH - chief cells in the parathyroid

187

3 ways PTH raises Ca

increases reabsorption in the bone (w/phosphate)
increases reabsorption in the kidney (distal convoluted tubule)
increase 1 alpha hydroxylase activity -> Vit D3 (calcitriol)

188

Regulation of PTH
Ca?

Mg?

Ca sensors on chief cells respond to low serum levels

low Mg levels also stimulate PTH release but prolonged low Mg leads to less PTH

189

Low Mg can affect what hormone?

Causes

PTH

diarrhea, aminoglycoside, diuretics, alcohol abuse

190

How does PTH increase Ca reabsorption from the bone

binds to osteoblasts which up regulate RANK L which then binds to osteoclasts stimulating Ca release

191

PTH role on phosphate?

Phosphate trashing hormone

192

Vitamin D's roll on Ca and phosphate (3)

Vitamin D increases Ca and Phosphate reabsorption from the gut

Vitamin D increases bone reabsorption of Ca and Phosphate

low Ca and Phosphate stimulate active Vit D

193

Ca and Phosphate differences w/ Vit D and PTH

Vit D
-increases Ca and phosphate reabsorption in the gut

PTH increases only Ca reabsorption in the gut

194

Most common cause of hypercalcemia ?

Consequences(4)

primary parathyroid adenoma
-

Stones
-renal stones/nephrocalcinosis/polyuria/uremia

Bones
-osteitis fribrosa cystica/osteoperosis/osteomalacia/osteoarthritis

Groans
-ab pain/constipation/peptic ulcers/pancreatitis

Psychiatric overtones
-lethargy/fatigue/depression/psychosis/ confusion

195

Malignancies associated w/ PTHrP

Squamous cell - lung
renal cell carcinoma
Breast cancer to METs

196

Why do you get peptic ulcers w/ hypercalcemia

stimulates gastrin production

197

four conditions associated w/ hypercalcemia

Stones
-renal stones/nephrocalcinosis/polyuria/uremia

Bones
-osteitis fribrosa cystica/osteoperosis/osteomalacia/osteoarthritis

Groans
-ab pain/constipation/peptic ulcers/pancreatitis

Psychiatric overtones
-lethargy/fatigue/depression/psychosis/ confusion

198

primary hyperparathyroidsm and secondary hyperparathyroidism have an increased lab value

alk phos

199

primary hyperparathyroidism lab value

Ca
alk phos
PTH
phosphate

High Ca
High Alk phos
High PTH
Low phosphate

200

secondary hyperparathyroidism lab value

Ca
alk phos
PTH
phosphate

Low Ca (drives PTH release)
alk phos is high
PTH is high
Phos is high (due to inability to excrete despite high PTH)

common cause is chronic renal failure, due to decrease gut Ca reabsorption and increased phosphate

201

most common cause of secondary hyperparathyroidism

chronic renal failure

202

refractory hyperparathyroidism is due to

lab values of Ca?

due to chronic renal failure, very high PTH despite having high Ca

203

Hypocalcemia is due to (4)

hypoparathyroidism
-accidental removal of parathyroids
-autoimmune destruction
-Degeorge
-Pseudohypoparathyroidism - kidneys unresponsive to PTH

Poor Ca intake

Vit D deficiency

Acute pancreatitis (Ca precipitates out FA -> soaps and excreted)

204

Causes of hypo parathyroidism -> hypocacemia

Accidental removal
autoimmune destruction
pseudohypoparathyroidism
DeGeorge syndrome

205

Pseudohypoparathyroidism due to?

See presentation?

Lab values of Ca and PTH

Albrights hereditary ostreodystophy

AD kidney unresponsive to PTH
-> High PTH
-> Low Ca due to loss in the kidney

shortened 4th and 5th digits
short stature
osteritis fibrosis cystica

206

what starts the intrinsic pathway?

release of tissue factor from a cell binding to factor VII

207

Thrombin does what in the coag pathway

what creates it?

prothrombin(factor II) -> thrombin via Xa
- Factor V serves as an excellent

thrombin converts fibrinogen to fibrin to create a mesh and stabilize clots

208

what blocks Thrombin?

Which drug stimulates this effect?

Antithrombin (antithrombin III)

heparin induces

209

Factor 12 encourages what 2 paths

1. starts the intrinsic pathway and begins its shut down

2. encourages conversion of prekallikrien -> kallikrein

kallikrein then
1. converts plasminogen -Plasmin
2.converts HMWK -> bradykinin
(vasodialation, permeability, pain)

210

where does bradykinin come from and what are its effects(3)?

Breakdown due to?

Kallikrien encourages conversion of HWMK -> bradykinin
- Vasodialation
-Permeability
- pain

Broken down by ACE enzyme

211

Hemophilia A is deficient in ?

Hemophilia B is deficient in ?

Alters PTT and PT how

A - 8
B - 9

longer PTT time w/ intrinsic factor modulation
no change in PT

212

Coagulation factors that serve as accelerants?

Modulator coag?

Factor 8a helps factor 9a activate factor 10 in the intrinsic pathway

Factor Va helps convert X -> Xa

Protein C and S deactivate the accelerants

213

Kallikrien's 2 functions

1. increases conversion of HMWK -> bradykinin

2. increases conversion of plasminogen ->plasmin

214

What additional components are needed in the coagulation cascade to assist (2)

Ca

phospholipids

215

PT measures what?

What is normal

measures the amount of time to clot after addition of tissue factor ( the extrinsic pathway -> uniquely VII) in addition to common path

1 is a normal INR

216

PTT measures what?

What is normal

PTT measures the amount of time to clot after adding something like silica, measures the intrinsic pathway (uniquely 12, 11, 9, 8) in addition to common path

normal is 35-40 seconds

217

Vitamin K deficiency has an effect on what coag factors?

What happens to PTT and PT?

Factors C, S
10, 9, 7, 2 are deficient

BOTH PTT and PT are elevated

218

macrohemmorrage such as hemarthrosis and easy bruising are due to defects in what?

coagulation cascade like hemophilia A or B

219

Factor V leiden deficency presents as?

Due to

most common form of hypercoagability

Factor 5 is mutated so protein C cannot shut down the cascade-> hypercoagable

220

Prothrombin G20210A is

G20210A

mutation in the 3' untranslated region of adenosine to guanine in prothrombin gene leading to increase production of prothrombin and hypercoagability

221

2 less common states of hypercoagability after factor V leiden and Prothrombin mutation?

Protein C/S deficiency -> less to inactivate factor V

Antithrombin deficiency -> less to inactivate Thrombin

222

What hypercoagable state may not be helped w/ thrombin?

antithrombin deficiency

223

Preferred anticoagulant during pregnancy?

Heparin or LMWH

224

Use of Heparin?

Immediate anticoag desired
-PE
-Acute coronary
-MI
-DV

Pregnancy

225

Platelets are decreasing after a new medication post an MI what is the drug?

MOA of toxicity

Heparin

Heparin induced thrombocytopenia, -> IgG antobodies bind to Heparin bound to Platelet factor 4
-> activation and clumping (hypercoagable)
-> eventual removal -> thrombocytopenia

226

Low molecular weight heparins (2)

enoxaparin
dalteparin

act more on factor Xa than antithrombin inducing

have better bioavailability

227

Toxicity w heparin (3)

Rx?

Bleeding
thrombocytopenia (Heparin induced thrombocytopenia)
osteoperosis

protamine sulfate

228

direct Xa blockers (2)

Argatroban
dabigatron

229

hirudin derived anticoags (3)

pepirudin
bivalirudin
desirudin

works by inhibiting thrombin ~ to natural antithrombin but dif MOA

230

skin tissue necrosis after a DVT be suspicious of what recently added drug?

Rx?

Warfarin

Give K either oral/IV

Fresh frozen plasma for immediate help

231

Follow what labs w/ warfarin?

w/ Heparin

follow INR/PT w/ warfarin

follow PTT w/ Heparin

232

Thrombolytics (4)

alteplase (tPA)
reteplase
tenecteplase
streptokinase

233

Clinical use of thrombolytic

see what lab values w/ PTT and PT?

converts plasminogen -> plasmin
-> increase PTT and PT

used in early MI (if no cath lab), early stroke, thrmbolysis of PE

234

Toxicity of thrombolytic

Rx

bleeding - do not use w/ a history of:
- recent surgery
- known bleeding dysarthria,
-HTN
-intracranial bleeding

Aminocapronic acid