Review Part 1 Flashcards
1
Q
What is needed for a diagnosis of DKA?
A
ketonemia and metabolic acidosis
2
Q
What is the management for DKA?
A
- insulin
- fluid replacement (normal saline) add 5% glucose once BG reaches 250 mg/dL
- replace potassium prophylactically with IV fluids
3
Q
What is HHNS (hyperosmolar hyperglycemic nonketotic syndrome)?
A
a state of severe hyperglycemia, hyperosmolarity, and dehydration
4
Q
Who is HHNS typically seen in?
A
elderly with type II diabetics
5
Q
What are common findings with HHNS?
A
CNS and focal neurologic signs
6
Q
What is the management for HHNS?
A
- fluid replacement is most important
- low-dose insulin infusion
7
Q
What are the autonomic complications of diabetes?
A
- impotence in men
- gastroparesis - chronic nausea and vomiting, early satiety
8
Q
What is the most common cause of end-stage renal disease?
A
diabetic nephropathy
9
Q
What is pathognomonic for DM?
A
nodular glomerular sclerosis - hyaline deposition in one area of glomerulus
10
Q
What increases the risk of progression of diabetic nephropathy to ESRD?
A
hypertension
11
Q
What is the treatment used to decrease the rate of progression of nephropathy
A
ACE inhibitor or ARB
12
Q
What is the leading cause of blindness in the US?
A
diabetic retinopathy
13
Q
What does fundoscopic examination show of diabetic retinopathy?
A
hemorrhages, exudates, micro aneurysms, and venous dilation
14
Q
What is the leading cause of visual loss in diabetic patients?
A
edema of the macula
15
Q
Peripheral Neuropathy
A
- AKA: distal symmetric neuropathy
- “stocking/glove pattern”
- begins in feet, later involves the hands
16
Q
What symptoms are common in peripheral neuropathy?
A
numbness and paresthesia
17
Q
Painful diabetic neuropathy
A
- hypersensitivity to light touch
- severe “burning” pain (especially at night)
18
Q
Treatment for diabetic neuropathy
A
pregablin, gabapentin, duloxetine, TCAs
19
Q
What Cranial Nerve is most often effected by diabetes?
A
CN III (oculomotor) -diabetic third nerve palsy
20
Q
What macrovascular complications is the most common cause of death in diabetic patients?
A
coronary artery disease
21
Q
What is the treatment of diabetic polyneuropathy?
A
- complex management
- pharmacologic agents: NSAIDs, pregablin, gabapentin, duloxetine, TCAs
- gastroparesis: promotility agent, such as metoclopramide, exercise, and low-fat diet
22
Q
What are the renal complications of diabetes?
A
diabetic nephropathy
23
Q
What is the prophylactic management of renal compilations of diabetes?
A
Control BP aggressively
-prescribe an ACE inhibitor or ARB if urine test is positive for microalbuminuria
24
Q
What are the manifestations of diabetes?
A
- polyuria (peeing a lot)
- polydipsia (constantly thirsty)
- polyphagia (constantly feeling the need to eat)
- fatigue
- weight loss
- blurred vision
- fungal infections
- numbness, tingling of hands and feet
25
What is normal Hemoglobin A1c value?
<5.6%
26
What is impaired fasting glucose Hemoglobin A1c value?
5.7% - 6.4%
27
What is diabetes Hemoglobin A1c value?
>6.5%
28
What is the somogyi effect?
glucose is low at 3 am glucose check
29
What is the treatment for somogyi effect?
evening insulin should be decreased
30
What is dawn phenomenon?
glucose is elevated at 3 am glucose check
31
What is the management of dawn phenomenon?
evening insulin should be increased to provide additional coverage in the overnight hours
32
What are the risk factors for diabetes?
- obesity (greatest risk factor)
- genetics
- age
- physical inactivity
33
How do you diagnosis diabetes?
perform any of the following tests on two separate days
- sxs of diabetes + a random glucose concentration of >200 mg/dL (not fasting)
- a fasting BG of >126 mg/dL
- a BG of >200 mg/dL 2 hours after a 75 g glucose load during an oral glucose tolerance test
34
What is the contraindications for metformin?
renal failure
35
What are the clinical manifestations of insulinoma?
sympathetic activation
-diaphoresis, palpitations, tremors, high blood pressure, anxiety
neuroglycopenic symptoms
-headache, visual disturbances, confusion, seizures, coma
36
What is the diagnosis for insulinoma?
-72 Hour Fast
Whipple Triad
- hypoglycemic symptoms brought on by fasting
- blood glucose <50 mg/dL during symptomatic attack
- glucose administration brings relief of symptoms
37
What is the mechanism of action of HMG CoA reductase inhibitors (statins)?
- rate-limiting step in cholesterol synthesis
| - deplete intracellular supply of cholesterol
38
What are the indications for high-intensity statin therapy?
- Clinical ASCVD + age <75
(and candidate for high-intensity statin)
- LDL >190 mg/dL
- Age 40 - 75 w/ type 1 or 2 DM + estimated 10 year ASCVD risk >7.5%
39
What is the medication effectiveness for high-intensity statin therapy?
daily doses lowers LDL-C by about 50% on average
40
What is the indication for moderate-intensity statin therapy?
- Established ASCVD risk >7.5%
| - Age 40-75 w/type 1 or 2 DM + no estimated 10 year ACVD risk >7.5%
41
What is the medication effectiveness for moderate-intensity statin therapy?
daily doses lowers LDL-C by 30-50% on average
42
What are the indications for low-intensity statin therapy?
for patients who cannot tolerate a high or moderate dose statin
43
What is the medication effectiveness of low-intensity statin therapy?
daily doses lowers LDL-C by less than 30% on average
44
What are the contraindications of statin therapy?
pregnancy category X
45
What are the side effects of statins?
- elevated liver function tests
| - myopathy and rhabdomyolysis
46
What is the most effective agent for increasing HDL-C?
nicotinic acid (niacin)
47
What is the MOA of nicotinic acid?
strongly inhibits lipolysis in adipose tissues, thereby reducing the free fatty acid production
48
What are the side effects of nicotinic acid?
- intense cutaneous flushing (with uncomfortable sensation of warmth) and pruritus
- hepatotoxicity
49
What is the mechanism of action of fibric acid derivatives?
- lowers serum triglycerides and increases HDL-C
| - fenofibrate >gemfibrizol in lowering triglyceride levels
50
What are the indications of fibric acid derivatives?
treatment of hypertriglyceridemia
51
What are the side effects of fibric acid derivatives?
- gallstone formation due to increased biliary cholesterol excretion
- contraindicated gemfibrizol + simvastatin
52
What is the mechanism of action for bile acid-binding resins?
- lowers bile acid concentration
| - keeps you from absorbing fats
53
What are the indications for bile acid-binding resins?
- cholestyramine can relieve pruritus related to bile acid accumulation in patients with biliary stasis
- colesevelam is also indicated for DMII due to glucose-lowering effects
54
What is the drug name in the Cholesterol Absorption Inhibitor class and ASEs?
- ezetimibe
| - adverse effects are uncommon
55
What is the MOA of Omega-3 Fatty Acids and what is the indication?
- MOA: inhibits VLDL and triglyceride synthesis in the liver
| - Lower triglyceride levels
56
What is the management for hypertriglyceridemia?
- primary therapy: diet and exercise
- secondary therapy: nicotinic acid and fibric acid derivatives are most effective
- omega-3 fatty acids in adequate doses may be beneficial
57
What are the laboratory testing done to look for complications from antihyperlipidemic agents?
- AST
- ALT
- CK levels
- eGFR
- INR
58
What are the physical exam findings related to hyperlipidemia?
- most patients are asymptomatic
- Xanthelasma: yellow plaques on eyelids
- Xanthoma: hard, yellowish masses found on tendons
59
What is the goal number for cholesterol?
< 200 mg/dL
60
What is high risk number for cholesterol?
> 240 mg/dL
61
What is goal number for HDL?
> 45 mg/dL (males)
| > 55 mg/dL (females)
62
What is a negative risk factor number for HDL?
> 60 mg/dL
63
What is high risk number for HDL?
< 40 mg/dL
64
What is goal number for LDL?
< 100 mg/dL
65
What is normal LDL for diabetics?
< 70 mg/dL
66
What is normal for triglycerides?
< 150 mg/dL
67
What are the causes of elevated LDL?
- hypertriglycerides
- low HDL levels
- obesity
- DM II
- metabolic syndrome
- infection or inflammatory states
68
What is the cause of elevated VLDL?
hypertriglycerides
69
What are the causes of elevated HDL?
- exercise
| - moderate consumption of alcohol
70
What are the causes of elevated triglycerides?
- DM
- obesity
- alcohol intake
- high fat meals lead to formation of large Chylomicrons particles due to the increased amount of triglyceride being transported
71
What medication has the best effect on elevated LDL?
statins
72
What are the potential complications of Statins?
- elevates liver function
- pregnancy category X
- myopathy and rhabdomyolysis
- increase effects of warfarin
73
What medication has the best effect on increasing HDL?
niacin
74
What are the potential complications of niacin?
- intense cutaneous flushing and pruritus
| - hepatotoxicity
75
What is the best treatment for isolate hypertriglyceridemia?
fibric acid derivatives (fenofibrate and gemfibrizol)
76
What are the potential complications of fibric acid derivatives?
- gallstone formation due to increased biliary cholesterol excretion
- gemfibrizol + simvastatin is contraindicated
77
What antihyperlipidemic drug is excreted by the kidneys?
nicotinic acid (niacin)
78
What antihyperlipidemic drug is excreted by the liver?
statins
79
What antihyperlipidemic drug is excreted by the feces?
bile acid-binding resins
80
What antihyperlipidemic is contraindicated for pregnancy?
HMG CoA Reductase inhibitors (statins)
81
Why are statins contraindicated during pregnancy?
cholesterol is an essential component of fetal development, including steroid synthesis and membrane development
82
What are high potency statins?
- rosuvastatin
| - atorvastatin
83
What are low potency statins?
- lovastatin
- fluvastatin
- pitavastatin
84
What is the MCC of Cushing's disease?
Pituitary adenoma
- producing large amounts of ACTH, which elevate cortisol.
- use MRI to visualize
85
What are pheochromocytomas? and what is the presentation of pheochromocytoma?
- Catecholamine producing tumors, Arise sporadically or inherited.
- palpitations
- headaches
- episodic sweating (diaphoresis)
86
What are the Rule of 10's for pheochromocytoma?
- 10% are bilateral
- 10% are extra-adrenal
- 10% are malignant
87
What is the presentation of Cushing's syndrome?
- fatty deposits between shoulders: buffalo hump and supraclavicular fat deposits
- rounded face: moon face
- pink or purple stretch marks: striae
- male pattern hair distribution (hirsutism)
- hypertension
- psych disturbances: depression, anxiety, euphoria, psychosis
88
What is the presentation of Addison's?
- hyperpigmentation
- insidious onset
- mood/personality change
- joint and muscle pain
- hypoglycemia
- fatigue
- weight loss
- vomiting, diarrhea
- headache
- sweating
89
What is the presentation of hirsutism?
androgen-dependent terminal hair (sexual hair) following a male-pattern hair growth
- face
- chest
- abdomen
- back
90
What are the hormones produced by adrenal medulla?
chromaffin cells of the medulla secrete both norepinephrine and epinephrin, but norepinephrine is usually the predominant amine
91
What are the hormones produced by adrenal cortex?
- mineralocorticoids: aldosterone
- glucocorticoids: cortisol
- adrenal androgen precursors: 5 androgens
92
What are the effects of androgens?
DHEA are converted in the gonads and peripheral target cells to sex steroids acting via androgen and estrogen receptors
93
What are the effects of mineralocorticoids and glucocorticoids?
regulate aspects of physiological stress, blood pressure, and electrolyte homeostasis
94
What labs are used to diagnosis pheochromocytoma?
Biochemical testing
-plasma and urine catecholamines and metanephrines: elevated
Imaging
- CT and MRI
- radioactive tracers can localize tumors
95
What labs are used to diagnose adrenal insufficiency?
ACTH (cosyntropin) stimulation test
- baseline ACTH and cortisol levels are drawn
- injection of cosyntropin, repeat cortisol levels at 30 and 60 minutes
- <18 = confirms insufficiency
Hyponatremia
96
What labs are used to diagnose Cushing's disease?
- late night salivary cortisol
- 24 hour urinary free cortisol excretion
- dexamethasone suppression test
97
Parathyroid hormone and how it interacts with vitamin D
- PTH acts directly on kidneys where it synthesizes 1,25-dihydroxyvitamin D hormone
- serum PTH levels are tightly regulated by a negative feedback loop where vitamin D is acting through its nuclear receptor to reduce PTH release and synthesis
- low vitamin D = high PTH
- high vitamin D = low PTH
98
What is the clinical presentation of hyperparathyroidism?
- stones: renal - loss of calcium and phosphate
- bones: pain - diffuse bone demineralization, trabecular bone increase
- groans: increased GI absorption and abdominal cramps
- moans: irritability and depression
99
What is the presentation of pseudohypoparathyroidism?
- short stature
- rounded face
- shortened 4th and 5th MCP
- obesity
- dental hypoplasia
- soft-tissue calcifications or ossifications
- developmentally delayed
100
What is the presentation of hypoparathyroidism?
- hypocalcemia (Chvostek's and Trousseau sign)
- muscle cramping
- paraesthesia in extremities
- hyperactive DTR's
- confusion
- seizures
101
How is Hirsutism graded?
Grade 0-4 (0 = no hirsutism, 4 = severe)
- > 9 in Mediterranean, Hispanic, and middle eastern
- > 8 in black and white
- > 6 South American
- > 2 in Asians
- 8-15 = mild
- 15-25 = moderate
- >25 = severe
102
What is Primary hyperaldosteronism?
Excess aldosterone secretion which is independent of renin-angiotensin system (Conn's Syndrome)
103
What are the causes of primary hyperaldosteronism?
- Aldosterone secreting adenoma (conns)
- Bilateral hyperplasia of the cortex
- Rarely carcinoma
104
What is the complete workup for cushing's?
- Determine if ACTH dependent or independent
- ACTH level <20 suggests adrenal tumor, hyperplasia or carcinoma
- Dexamethasone suppression test: Serial measurements of 2 or 3, 24hr urinary free cortisol
- MRI: if pituitary tumor suspected (Cushing’s Dz)
- CT: if Adrenocortical or other tumor suspected (Cushing’s Syndrome)
- Endocrine referral
105
What is the high dose and low dose dexamethasone suppression test observing?
High dose: assess between ectopic ACTH and Cushing’s disease:
- Ectopic ACTH tumor: Suppression absent
- Cushing’s disease: suppression (of ACTH and cortisol) present
Low dose: R/o pseudo-crushing’s syndrome:
- Healthy pt: Suppression present
- Cushing syndrome: Suppression absent
106
Where is hyperpigmentation usually found in a pt with Addisons?
- Palmar creases
- Buccal mucosa
- Vermilion border of the lips
- Around scars
- Nipples
107
What are the lab results for a pt w/ Addisons?
- Low serum cortisol levels at 8 a.m. < 3 mcg/dL
- Hyponatremia
- Hyperkalemia
- Elevated plasma renin level
- Increase in ACTH
108
What is the tx for Addisons?
Hydrocortisone, Fludrocortisone, DHEA(for women)
109
What are the sxs of Addisonian Crisis?
Adrenal insufficiency presenting as
- Shock
- HypoTN
- Weakness
- Abdominal pain
- N/V
- Confusion
- Volume depletion
110
Addisonian Crisis may occur in pts with?
Primary adrenal insufficiency who have been subjected to:
- Serious infxn or other major stress
- Bilateral adrenal infarction/hemorrhage
- Abrupt w/d from glucocorticoid therapy
111
What is the tx of Addisonian Crisis?
1mg ACTH stimulation test: plasma cortisol level is drawn at baseline and 30 minutes
- <25 and <9 elevation over baseline = inadequate adrenal response
DO NOT delay therapy while waiting for response
112
What is the difference between a macroadenoma and a microadenoma in a pt presenting with a pituitary adenoma?
- Macroadenoma: greater than 1 cm
| - Microadenomas: less than 1 cm
113
What is the MC secretory pituitary adenoma?
Prolactinomas
114
What are the sxs of a Prolactinoma?
- Irregular menstrual periods
- HA
- Fatigue
- Breast discharge
- Vision loss: Bitemporal hemianopsia (optic chiasms)
115
What is the management of a Prolactinoma?
- Get MRI and full endocrine testing and therapy
- Tx: Dopaminergic drug: Bromocriptine and Cabergoline.
- Surgical: TSS
116
What is a common DDx of Pheochromocytoma?
Panic Attacks
117
What are the S/Sxs and lab results of primary hyperaldosteronism?
S/Sxs: HTN and Hypokalemia
| Labs: increased aldosterone and low renin
118
What are the side effects of bile-acid binding resins?
GI-related: constipation, nausea, flatulence
