Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

USLME Kiss my ass and pray > endo DIT > Flashcards

endo DIT Flashcards

(234 cards)

Start Studying
1
Q

cAMP modifying hormones (11)

A 
FSH
LH
TSH
hCG
ACTH
MSH
GHRH
PTH
Calcitonin
glucagon
V2 vassopressin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

IP3 modifying hormones(4)

A

GNRH
TRH
Oxytocin
vasopressin (v1)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Tyrosine kinase receptor modulators

A 
GH
Insulin
insulin like growth factor
Platelet derived growth factor
fibroblast growth factor
Cytokines
prolactin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

cGMP modulators (2)

A

NO
ANP

the vasodialators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

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

A

binding globulin decreasing the amount of free active hormone

Thyroid - TGH for example

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Steroid receptor modulated hormone (5)

A 
estrogen, progesteron, testosterone
glucocorticoids
aldosterone
Thyroid hormone
Vit D
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Availabilty of binding hormone affects 2 things

A

amount of free hormone

activity of steroid hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

increased sex binding hormone may have what affect on men?

A

gynectomastia due to decreased free testosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

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

A

hurtusism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

ACTH and MSH are synthesized by what precursor?

Clinical relevance?

A

POMC

Leads to hyperpigmentation w/ primary adrenal insufficency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hyperprolactenima due to? (4)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Symptoms of hyperprolactinemia in

pre meno women

post meno?

Men

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Clinical uses of octreotide(3)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

infertility, galactorrhea and bitemporal hemanopsia

A

prolactinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

inability to breastfeed, amenorrhea, cold intolerance

A

sheehan syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Which hormones share a common alpha subunit(4)

A

TSH
LH
FSH
b hCG

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

anterior pituitary is derived from

A

rathke’s pouch

surface ectoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

posterior pituitary is derived from

A

neuroectoderm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

ADH is stimulated w/ ?(3)

Decreased w?(3)

A

nicotine
opiates
high serum osmolarity
low volume contraction

ethanol
atrial naturetic factor
low serum osmolarity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Oxytocin important w/

stimulated w?

A

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

cervical dilation
inhibited w/ alcohol and stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

inhibit feeds back and blocks

A

FSH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

progesterone and testosterone feedback on

A

LH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

ACTH is stimulated to release w/(2)

A

Stress

CRH from the hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

TSH is released from?

inhibited by?

Stimulated by?

A

TSH from the pituitary

inhibited by T3 and T4 levels

Stimulated by TRH from hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

USLME Kiss my ass and pray (33 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions