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Quarter 3 Finals > Clin Med > Flashcards

Clin Med Flashcards

1
Q

Overweight

A

BMI 25-29.9

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2
Q

Obese

A

BMI 30+

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3
Q

BMI

A

weight (kg) / height (m^2)

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4
Q

When to measure waist circumference?

A

If BMI b/w 25-35

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5
Q

Increased cardiometabolic risk based on Weight circumference

A

M: 40+ inches
F: 35+ inches

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6
Q

Increased cardiometabolic risk based on Weight circumference (Asian)

A

M: 35.4+ inches
F: 31.5+ inches

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7
Q

As people lose weight

A

metabolism tends to slow down, making it harder to continue losing weight

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8
Q

How to lose weight by creating negative energy balance

A

Crease 500-1000 calorie per day deficit= 1-2 lbs of weight loss per week

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9
Q

Goals of weight loss

Initial goal:

A

5-7% of body weight

loss of >5% reduces risk factors for CVD

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10
Q

Commonly rec diets for weight loss and protection against DM and CAD

A

Mediterannean: low meat, fat is from olive oil, plant based

DASH (to stop HTN): veggies, fruit, low fat dairy, whole grains, fish, poultry, buts

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11
Q

Recommended for all of the following: Type 2 DM, CVD, Kidney dz

A

DASH

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12
Q

Intermittent fasting

A

Promote weight loss
Improves lipids
Reduces BP, fasting BS, and A1C

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13
Q

Obesity screening

A

Screen ALL Adults

if BMI 30+: refer for intensive, multicomponent behavioral intervention

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14
Q

If diagnosed obese, what is considered comprehensive and high intensity intervention?

A

2x/month for at least 3 months

12-26 sessions/year

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15
Q

The most important factor in a lifestyle change plan

A

Readiness to change

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16
Q

Low risk

A

BMI 25-29.9 with NO CVD, Risk factors, or other comorbidities

Tx: diet/exercise counseling

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17
Q

Moderate risk

A

BMI 25-29.9 AND 1 or more Risk factor
OR
BMI 30-34.9

Tx: intensive, multicomponent behavior modification + drug therapy for SOME

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18
Q

High risk

A

BMI 35-40

Intensive, multicomponent behavior modification + consider drug therapy or Surgery

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19
Q

Very high risk

A

BMI >40

Intensive, multicomponent behavior therapy + consider drug therapy or Surgery

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20
Q

When to consider meds for Obesity

A

BMI 30+ or >27 with comorbidity

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21
Q

When to consider meds for Obesity

A

AFTER 3-6 months, if <5% weight loss has been achieved

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22
Q

Goals of drug therapy

A

reduce weight by 4-8% within 6-12 months

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23
Q

Orlistat (Alli/Xenical)

A

Inhibit pancreatic lipase, altering fat digestion

Fatty stools, Unpleasant GI SE

Take Vitamin!! (may decrease absorption of fat soluble vitamins, ADEK)

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24
Q

Liraglutide (Victoza)

A

GLP-1 RA
(also a DM drug, Type 2)
Daily SQ injection

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25
Q

Phentermine/ Topiramate

A

DO NOT USE in pts with HTN, CAD, or Hyperthyroid

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26
Q

Phentermine

A

Symp-mimetic
DO NOT USE in pts with HTN, CAD, or Hyperthyroid

only FDA app for short term- 12 wks
The most widely prescribed wt loss drug

More SE- careful with addictive personalites

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27
Q

Bariatric surgery

A

Efficient, improve DM and HTN, lower long term mortality rates

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28
Q

Consider bariatric surgery with

A

BMI 40+
BMI 35-40 AND 1 or more other serious comorbidity
BMI 30-35 AND uncontrollable DM2 or Metabolic syndrome

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29
Q

Why is it important to lose weight before bariatric surgery?

A

Loss of 8% excess body weight prior to surgery leads to greater weight loss post op

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30
Q

CONTRA-indications to bariatric surgery

A 
Eating disorder
Untreated mental illness
Drug/Alc abuse
Coagulopathy
Severe cardiac dz
Cannot comply w new diet
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31
Q

Bariatric surgery can cause wt loss in many ways:

A

Restriction (make stomach smaller)
Malabsorption (make small bowel shorter)
Decrease appetite/ improve metabolsim (change release of hormones)

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32
Q

Exercise recommendation

aerobic

A

150-300 min of MODERATE

OR

75-150 min of VIGOROUS

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33
Q

Exercise recommendation

muscle strengthening

A

2 or more days/week

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34
Q

Hormones released from Ant Pit (6)

A 
ACTH
TSH
LH
FSH
GH
Prolactin
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35
Q

Ant Pit

A

Makes AND Secretes hormones in response to negative fdback from Adrenal, Thyroid, and Gonads

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36
Q

ACTH

A

stimulates production and release of Cortisol

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37
Q

LH in females

A

Triggers ovulation (LH Surge) and development of Corpus Luteum

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38
Q

LH in males

A

Tells Leydig cells to produce Testosterone

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39
Q

FSH in females

A

Growth of ovarian follicles

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40
Q

FSH in males

A

formation of Secondary spermatocytes

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41
Q

Prolactin in males

A

Work with LH and Testosterone to increase reproductive function

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42
Q

Posterior pit

A

ONLY RELEASES hormones that are made in hypothalamus

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43
Q

Intermediate pituitary
AKA
“Pars Intermedia”

A

MAKES and SECRETES Melanocyte stimulating hormone- skin pigmentation

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44
Q

ACTH made by

A

Corticotrophs

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45
Q

TSH made by

A

Thyrotrophs

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46
Q

LH and FSH made by

A

Gonadotrophs

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47
Q

GH made by

A

Somatotrophs

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48
Q

Prolactin made by

A

Lactotrophs

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49
Q

Sellar Mass clinical sx

A

Visual, diplopia, HA

Incidental finding on MRI

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50
Q

Why does visual change occur w Sellar mass?

A

Suprasellar extension of adenoma compressing the Optic Chaism
“Bitemporal hemianopsia”
AKA tunnel vision

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51
Q

Type of Sellar mass: Benign Tumor

A

Pituitary adenoma is a type of BENIGN

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52
Q

Most common Pituitary adenoma (a benign Sellar mass)

A

Prolactinoma

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53
Q

Clinical sx of Prolactinoma in pre-menopausal women

A

No period
Infertile
Galactorrhea
Serum prolactin level: >30

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54
Q

Clinical sx of Prolactinoma in post-menopausal women

A

HA
Impaired vision
Galactorrhea
Serum prolactin level >20

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55
Q

Clinical sx of Prolactinoma in Men

A

Decreased libido
ED, infertile
Gyencomastea
Serum prolactin level >20

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56
Q

Tx of Prolactinoma

A

Cabergoline (pharm)
OR
Transsphenoidal resection (standard of care)

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57
Q

GH excess most common cause

A

Benign pituitary macroadenoma (from somatotrophs)

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58
Q

Acromegaly

A

ADULTS

Increased risk of DM, HTN, and CAD

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59
Q

Growth Hormone Excess Dx

A

OGTT: >1 after two hours
GOLD STANDARD

Can also do IGF-1 levels, MRI

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60
Q

Tx of GH excess

A

Transsphenoidal Microsurgery: most successful in pts iwth GH <50 and tumor <2cm

Pharm: Somatostatin analog (Octreotide/lanreotide)

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61
Q

Monitoring of GH excess

A

IGF-1 levels every 3-6 months

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62
Q

GH deficiency (not enough)

A

Pit adenoma or after tx of tumor (removed too much)

Rare: Sheehan synd

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63
Q

GH deficiency in adults

A

Tumors are #1 cause

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64
Q

Tx of GH deficiency in adults

A

Only warranted if they have hx of childhood onset GH deficiency

Tx: daily injections of GH

65
Q

Primary Hypogonadism

Hyper Hypo

A

problem with testis

Low testosterone
High FSH and LH

66
Q

Secondary hypogonadism

Hypo Hypo

A

problem with Ant Pit

Low testosterone
Low/norm FSH and LH

67
Q

Secondary hypogonadism (Ant Pit is problem)

Hypo Hypo

Clinical sx:

A

ED, hot flash, gynecomastia, infertile, dec energy and libido, dec muscle mass and body hair

Dx: free and total Testosterone, LH and FSH

68
Q

If diagnosed Secondary Hypo (Hypo hypo),

A

test all other Ant pit hormones to make sure the entire Ant Pit is not broken

69
Q

Tx for Hypo Hypo

A

IM injections every 2 wks
Transdermal cream/gel/patch daily
Pellets every 3 months

70
Q

Hypo Hypo management

A

B4 tx: Rectal exam and PSA

Monitoring: Free and total T, CBC, Free Estradiol, Annual rectal and PSA

71
Q

CONTRA to treating Hypo Hypo with testosterone

A

Hx of Prostate CA

72
Q

Pan-Hypopituitarism

A

ENTIRE Ant Pit is not fx correctly, causing decrease of all hormones

Etiology: radiation (50%), tumor, Sheehan synd (rare)

73
Q

Sheehan synd

A

Postpartum necrosis of Ant Pit d/t blood loss or shock

74
Q

Most common initial sx of Sheehan

A

Agalactorrhea/ difficulties with breastfeeding

75
Q

Dx of Sheehan syn

A

Hx and PE
Full hormone workup
MRI brain
Stimulation test

76
Q

Tx of Sheehan

A

Extensive hormone replacement

Levothyroxine- thyroid, Dexamethasone- cortisol, T, Estrogen, GH, Ca and Vit D

77
Q

Central Diabetes Insipidus

A

not enough ADH

  • a lot of dilute urine
  • thirsty
  • nocturia/enuresis
78
Q

SIADH

A

too much ADH

-little urine, very concentrated

79
Q

Tx of Central Diabetes Insipidus

A

Desmopressin

available intranasally

80
Q

Dx of both Central DI and SIADH

A

24 hr urine collection

With SIADH, also r/o CNS disorder and lung tumor w CT/MRI of head and CXR

81
Q

Tx of SIADH

A

fluid restriction

82
Q

Low dose Dexamethasone suppression test

A

Cushing synd

83
Q

Cosynotropin (synthetic ACTH) Stimulation test

A

Addison’s dz

84
Q

Clonidine suppression test

A

Pheochromocytoma

85
Q

Aldosterone is regulated by

A

AT II
Serum K
ACTH

86
Q

Cortisol

A

glucose regulation

87
Q

Cushing synd (too much cortisol)

A 
Stria
Hyperpigmentation
Moon face
Buffalo hump
HTN
Osteroporosis
Depression/Anxiety
Amenorrhea
Hirsuitism, Acne, increased libido
88
Q

Cushing DISEASE

A

Pituitary hypersecretion of ACTH (very common, 70% of all Cushings syndrome)

89
Q

ACTH dependent (more common, 80% of all cushings)

A

ACTH is HIGH

Female to male 8:1

90
Q

ACTH independent

A

often from steroid use

pheochromocytoma

91
Q

Diagnosing Cushing

A
  1. 24 hr urine free Cortisol (GOLD STANDARD)

1. then, Low dose dexamethasone suppression test

92
Q

Low dose dexamethasone suppression test

A

Give 1 mg dexamethasone at 11 pm
Measure cortisol in morning, if >5 (abnormal)

SUSPICIOUS FOR ACTH INDEPENDENT, bc ACTH is not listening to high Cortisol levels

93
Q

Pharm tx for Cushing

A

1st line: Ketoconazole

94
Q

If Ketoconazole is not enough for Cushing dz

A

Add Metyrapone

95
Q

Conn syndrome

A

Primary hyperaldosteronism

Bilateral hyperplasia (more common)
Unilateral tumor
96
Q

When to be suspicious

A

Low K

HTN

97
Q

Lab testing for Conn synd (hyperaldosteronism)

A
  1. Increased Aldosterone in plasma
  2. Decreased Renin in plasma
  3. Spontaneous Hypokalemia
98
Q

Tx of Conn synd (hyperaldosteronism)

A

Unilateral tumor: remove

Bilateral hyperplasia: Spironolactone

99
Q

Addison’s dz

A

LOW EVERYTHING
Low Aldo: Hyperkalemia, Hypotension, Acidosis, Salt craving

Low cortisol: hypoglycemia, wt loss, musc weak
Low androgen: dec libido and pubic hair

Increased ACTH: Hyperpigmentation

100
Q

Secondary and tertiary insuff

A

will not have any Aldo sx (Aldo is normal)

No hyperpigmentation

101
Q

Secondary

A

low ACTH

102
Q

Tertiary

A

low CRH

103
Q

Cause of Addisons (low everything)

A

Auto-immune destruction of Adrenal Cortex

104
Q

Cause of Secondary and Tertiary insufficiency

A

Abrupt cessation of Exogenous steroids is most common cause of Secondary

105
Q

Dx Adrenal Insufficiency

A

Serum morning Cortisol

Cosyntropin ACTH Stimulation test - find out where defect is

106
Q

Cosyntropin ACTH test

A

Draw baseline cortisol
Give bolus of Cosyntropin
Measure Cortisol again 30-60 min later

If Cortisol can’t raise 7 above baseline OR >18, there is ADDISONS

107
Q

Tx Addisons

A

Short acting steroid (hydrocortisone)

Long acting (Dexamethasone, prednisone)

Mineralcorticoid (if need estrogen replacement)
Consider oral DHEA for women

108
Q

Pheo

A

Classic triad:
HA
Sweating
Tachycardia

109
Q

Pheo tumors are usually

A

BENIGN 90%

usually arise from Adrenal Medulla

110
Q

When to suspect pheo

A

Paroxysmal “attach”
Refractory/persistent HTN
Onset HTN <20 YO
Family hx of pheo

111
Q

Dx of Pheo

A

Plasma metanephrines
24 hr urine: VMA
Clonidine suppression test

112
Q

Pheo dx

A

After labs, CT scan of abdomen WITHOUT contrast

113
Q

Tx of Pheo

A

A-blocker (Phenoxybenzamine) and B-blocker (Propranolol)

SURGERY is definitive

114
Q

Adrenal incidentaloma

A

> 1 cm

115
Q

For all pts w/ adrenal incidentaloma

A

R/o Pheo and Cushing

116
Q

Pt has Adrenal Incidentaloma and HTN

A

R/o primary Hyperaldosteronism “Conn Synd”

117
Q

Pt has Adrenal Incidentaloma and primary CA

A

DO NOT BIOPSY if suspect pheo or known METs

118
Q

Adrenal incidentaloma workup is negative, likely benign, and mass is <2 cm

A

repeat imaging at 6 months

Repeat Dexamethasone suppression test (cushing test) yearly x 4 years

119
Q

If workup negative, likely benign, BUT mass is >2cm

A

Consider SURGERY

120
Q

Type 1 DM prone to other Auto-immune disorders

A

Thyroid dz, Celiac, Pernicious Anemia

121
Q

Clinical sx of Type 1

A 
3 Ps
Weight loss
Nocturia
Blurry vision
DKA
Fatigue
Paresthesias 
Infections- candida
122
Q

Type 2 DM

A

Gradual onset

Genetic PreD is higher

123
Q

Progression of Type 2 DM

A

Peripheral insulin resistance –> Impaired glucose tolerance –> Overt diabetes –> Beta cell failure “burnout”

124
Q

Clinical sx of Type 2

A

Asymptomatic, OR

Polyuria, polydipsia
Blurred vision
Acanthosis Nigricans
Chronic skin infection
Vulvovaginitis, Balanitis
125
Q

Screening for DM

A

Anyone overweight by BMI: 25 or more (23 or more in Asians) with 1 or more risk factors

and

ALL pts 45+ YO

126
Q

Fasting plasma glucose

A

> 126 is DM

127
Q

2 hr Oral Glucose Tol Test- OGTT

A

200+ is DM

128
Q

A1C%

A

> 6.5% is DM

129
Q

Normal A1C

A

<5.7%

130
Q

Random plasma glucose

A

> 200 AND classic DM sx is diagnosable

131
Q

To diagnose Acute onset Type 1 DM with sx of hyperglycemia,

A

Blood glucose should be used rather than A1C

132
Q

Pre Diabetes

A

Fasting: 100-125
2 hr: 140-199
A1C: 5.7%-6.4%

133
Q

Consider Metformin for Pre-diabetic ESP IF

A

BMI >35
age 60+ YO
Women w hx of Pregestational DM

134
Q

ASCVD (3 parts)

A

Coronary Heart Dz
Cerebrovascular Dz
Peripheral Artery Dz

135
Q

Tx for ASCVD

A

Lifestyle
BP management
Lipid management
Antiplatelet (ASA or Colopidogrel/Plavix)

136
Q

Diabetic Nephropathy
AKA
“Diabetic Kidney Dz”

A

occurs in 20-40% of pts with DM

Related to chronic hyperglycemia

137
Q

Diabetic Nephropathy “Diabetic Kidney Dz”

A

typically after 10 yrs in type 1, may be present at Dx in Type 2

138
Q

Clinical sx of Diabetic nephropathy “Diabetic Kidney dz”

A

Albuminuria
Reduced eGFR
(absence of another cause for the kidney damage)

139
Q

Clinical progression of Diabetic Kidney dz

A

Long standing DM: progressive Albuminuria >300, HTN, and decline in GFR

140
Q

Screen for Diabetic Nephropathy

A

AT least ONCE/YR
Urinary ACR
2-3 specimens of UACR within 3-6 month period have to be abnormal before diagnosing

141
Q

Screen for Diabetic Nephroparhy

A

after 5 years of Type 1

immediately for Type 2

142
Q

Tx for Diabetic Nephroparhy

A

ACE-I and ARBs

Intense glycemic and BP control

143
Q

Diabetic Retinopathy

A

Highly specific vascular complication with Type 1 and 2

leading cause of blindness b/w age 20-74 in the US

144
Q

Prevalence of DM Retinopathy related to

A

Duration AND level of glycemic control

145
Q

Other Risk Factors for Diabetic Retinopathy

A

Nephropathy
HTN
Dyslipidemia

146
Q

Two types of Diabetic Retinopathy

A

Non-prolif and Prolif

147
Q

Non-proliferative DM Retinopathy

A

“Cotton wool spots”
Retinal hemorrhage
yellow lipid exudate

148
Q

Proliferative DM

A

NEW VASCULATURE

neovascularization

149
Q

Clinical sx of Diabetic Retinopathy

A

often NONE until late dz

Refer to Ophtho!!!

150
Q

Screening for DM Retinopathy

A

Type 1: within 5 yrs of dx

Type 2: immediately

151
Q

Diabetic Retinopathy after screening

A

If no sx for at least 1 annual exam and sugars well controlled, can then screen every 1-2 years

152
Q

If any level of Diabetic Retinopathy is present

A

Sequental dilated retinal exam AT LEAST ANNUALLY

153
Q

Diabetic Neuropathy

A

Peripheral vs Autonomic

154
Q

Peripheral Neuroparhy

A

“Stocking glove”
Pain, numbness, LOPS (loss of protective sensation) Risk for ulcers
Loss of vibratory, proprioception

Decreased or absent ankle reflexes

155
Q

Foot ulcers Risk Factors

A 
Hx of ulcer
LOPS
Foot deformity: Charcot foot
PAD
Poor glycemic control
Callus or corn
CKD (esp on dialysis)
156
Q

Comprehensive foot exam

A 
AT LEAST ANNUALLY
Type 1: start @ 5 yr 
Type 2: immediately
Hx, inspection, VASCULAR 
-DP and PT pulse
-ABI if sx of claudication or decreased pulse 
NEURO
-10 g monofilament protective sensation test
157
Q

ABI

A

ankle brachial index

158
Q

Autonomic Neuropathy

A 
Hypoglycemia unawareness***
Orthostatic hypotension
Gastroparesis***
Sexual dysfx
Incontinence
Diarrhea/constipation
Anhidrosis- sweating issues
Abnormal pupillary response
159
Q

Referrals for DM

A 
Eye
Family planning
Dietician
Diabetes self management
Dentist
Podiatrist
Mental health professional

Quarter 3 Finals (10 decks)

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