Clin Med Flashcards
1
Q
Overweight
A
BMI 25-29.9
2
Q
Obese
A
BMI 30+
3
Q
BMI
A
weight (kg) / height (m^2)
4
Q
When to measure waist circumference?
A
If BMI b/w 25-35
5
Q
Increased cardiometabolic risk based on Weight circumference
A
M: 40+ inches
F: 35+ inches
6
Q
Increased cardiometabolic risk based on Weight circumference (Asian)
A
M: 35.4+ inches
F: 31.5+ inches
7
Q
As people lose weight
A
metabolism tends to slow down, making it harder to continue losing weight
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
9
Q
Goals of weight loss
Initial goal:
A
5-7% of body weight
loss of >5% reduces risk factors for CVD
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
11
Q
Recommended for all of the following: Type 2 DM, CVD, Kidney dz
A
DASH
12
Q
Intermittent fasting
A
Promote weight loss
Improves lipids
Reduces BP, fasting BS, and A1C
13
Q
Obesity screening
A
Screen ALL Adults
if BMI 30+: refer for intensive, multicomponent behavioral intervention
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
15
Q
The most important factor in a lifestyle change plan
A
Readiness to change
16
Q
Low risk
A
BMI 25-29.9 with NO CVD, Risk factors, or other comorbidities
Tx: diet/exercise counseling
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
18
Q
High risk
A
BMI 35-40
Intensive, multicomponent behavior modification + consider drug therapy or Surgery
19
Q
Very high risk
A
BMI >40
Intensive, multicomponent behavior therapy + consider drug therapy or Surgery
20
Q
When to consider meds for Obesity
A
BMI 30+ or >27 with comorbidity
21
Q
When to consider meds for Obesity
A
AFTER 3-6 months, if <5% weight loss has been achieved
22
Q
Goals of drug therapy
A
reduce weight by 4-8% within 6-12 months
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)
24
Q
Liraglutide (Victoza)
A
GLP-1 RA
(also a DM drug, Type 2)
Daily SQ injection
25
Phentermine/ Topiramate
DO NOT USE in pts with HTN, CAD, or Hyperthyroid
26
Phentermine
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
27
Bariatric surgery
Efficient, improve DM and HTN, lower long term mortality rates
28
Consider bariatric surgery with
BMI 40+
BMI 35-40 AND 1 or more other serious comorbidity
BMI 30-35 AND uncontrollable DM2 or Metabolic syndrome
29
Why is it important to lose weight before bariatric surgery?
Loss of 8% excess body weight prior to surgery leads to greater weight loss post op
30
CONTRA-indications to bariatric surgery
```
Eating disorder
Untreated mental illness
Drug/Alc abuse
Coagulopathy
Severe cardiac dz
Cannot comply w new diet
```
31
Bariatric surgery can cause wt loss in many ways:
Restriction (make stomach smaller)
Malabsorption (make small bowel shorter)
Decrease appetite/ improve metabolsim (change release of hormones)
32
Exercise recommendation
| aerobic
150-300 min of MODERATE
OR
75-150 min of VIGOROUS
33
Exercise recommendation
| muscle strengthening
2 or more days/week
34
Hormones released from Ant Pit (6)
```
ACTH
TSH
LH
FSH
GH
Prolactin
```
35
Ant Pit
Makes AND Secretes hormones in response to negative fdback from Adrenal, Thyroid, and Gonads
36
ACTH
stimulates production and release of Cortisol
37
LH in females
Triggers ovulation (LH Surge) and development of Corpus Luteum
38
LH in males
Tells Leydig cells to produce Testosterone
39
FSH in females
Growth of ovarian follicles
40
FSH in males
formation of Secondary spermatocytes
41
Prolactin in males
Work with LH and Testosterone to increase reproductive function
42
Posterior pit
ONLY RELEASES hormones that are made in hypothalamus
43
Intermediate pituitary
AKA
"Pars Intermedia"
MAKES and SECRETES Melanocyte stimulating hormone- skin pigmentation
44
ACTH made by
Corticotrophs
45
TSH made by
Thyrotrophs
46
LH and FSH made by
Gonadotrophs
47
GH made by
Somatotrophs
48
Prolactin made by
Lactotrophs
49
Sellar Mass clinical sx
Visual, diplopia, HA
| Incidental finding on MRI
50
Why does visual change occur w Sellar mass?
Suprasellar extension of adenoma compressing the Optic Chaism
"Bitemporal hemianopsia"
AKA tunnel vision
51
Type of Sellar mass: Benign Tumor
Pituitary adenoma is a type of BENIGN
52
Most common Pituitary adenoma (a benign Sellar mass)
Prolactinoma
53
Clinical sx of Prolactinoma in pre-menopausal women
No period
Infertile
Galactorrhea
Serum prolactin level: >30
54
Clinical sx of Prolactinoma in post-menopausal women
HA
Impaired vision
Galactorrhea
Serum prolactin level >20
55
Clinical sx of Prolactinoma in Men
Decreased libido
ED, infertile
Gyencomastea
Serum prolactin level >20
56
Tx of Prolactinoma
Cabergoline (pharm)
OR
Transsphenoidal resection (standard of care)
57
GH excess most common cause
Benign pituitary macroadenoma (from somatotrophs)
58
Acromegaly
ADULTS
| Increased risk of DM, HTN, and CAD
59
Growth Hormone Excess Dx
OGTT: >1 after two hours
GOLD STANDARD
Can also do IGF-1 levels, MRI
60
Tx of GH excess
Transsphenoidal Microsurgery: most successful in pts iwth GH <50 and tumor <2cm
Pharm: Somatostatin analog (Octreotide/lanreotide)
61
Monitoring of GH excess
IGF-1 levels every 3-6 months
62
GH deficiency (not enough)
Pit adenoma or after tx of tumor (removed too much)
| Rare: Sheehan synd
63
GH deficiency in adults
Tumors are #1 cause
64
Tx of GH deficiency in adults
Only warranted if they have hx of childhood onset GH deficiency
Tx: daily injections of GH
65
Primary Hypogonadism
Hyper Hypo
problem with testis
Low testosterone
High FSH and LH
66
Secondary hypogonadism
Hypo Hypo
problem with Ant Pit
Low testosterone
Low/norm FSH and LH
67
Secondary hypogonadism (Ant Pit is problem)
Hypo Hypo
Clinical sx:
ED, hot flash, gynecomastia, infertile, dec energy and libido, dec muscle mass and body hair
Dx: free and total Testosterone, LH and FSH
68
If diagnosed Secondary Hypo (Hypo hypo),
test all other Ant pit hormones to make sure the entire Ant Pit is not broken
69
Tx for Hypo Hypo
IM injections every 2 wks
Transdermal cream/gel/patch daily
Pellets every 3 months
70
Hypo Hypo management
B4 tx: Rectal exam and PSA
| Monitoring: Free and total T, CBC, Free Estradiol, Annual rectal and PSA
71
CONTRA to treating Hypo Hypo with testosterone
Hx of Prostate CA
72
Pan-Hypopituitarism
ENTIRE Ant Pit is not fx correctly, causing decrease of all hormones
Etiology: radiation (50%), tumor, Sheehan synd (rare)
73
Sheehan synd
Postpartum necrosis of Ant Pit d/t blood loss or shock
74
Most common initial sx of Sheehan
Agalactorrhea/ difficulties with breastfeeding
75
Dx of Sheehan syn
Hx and PE
Full hormone workup
MRI brain
Stimulation test
76
Tx of Sheehan
Extensive hormone replacement
| Levothyroxine- thyroid, Dexamethasone- cortisol, T, Estrogen, GH, Ca and Vit D
77
Central Diabetes Insipidus
not enough ADH
- a lot of dilute urine
- thirsty
- nocturia/enuresis
78
SIADH
too much ADH
| -little urine, very concentrated
79
Tx of Central Diabetes Insipidus
Desmopressin
available intranasally
80
Dx of both Central DI and SIADH
24 hr urine collection
With SIADH, also r/o CNS disorder and lung tumor w CT/MRI of head and CXR
81
Tx of SIADH
fluid restriction
82
Low dose Dexamethasone suppression test
Cushing synd
83
Cosynotropin (synthetic ACTH) Stimulation test
Addison's dz
84
Clonidine suppression test
Pheochromocytoma
85
Aldosterone is regulated by
AT II
Serum K
ACTH
86
Cortisol
glucose regulation
87
Cushing synd (too much cortisol)
```
Stria
Hyperpigmentation
Moon face
Buffalo hump
HTN
Osteroporosis
Depression/Anxiety
Amenorrhea
Hirsuitism, Acne, increased libido
```
88
Cushing DISEASE
Pituitary hypersecretion of ACTH (very common, 70% of all Cushings syndrome)
89
ACTH dependent (more common, 80% of all cushings)
ACTH is HIGH
| Female to male 8:1
90
ACTH independent
often from steroid use
| pheochromocytoma
91
Diagnosing Cushing
1. 24 hr urine free Cortisol (GOLD STANDARD)
| 1. then, Low dose dexamethasone suppression test
92
Low dose dexamethasone suppression test
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
Pharm tx for Cushing
1st line: Ketoconazole
94
If Ketoconazole is not enough for Cushing dz
Add Metyrapone
95
Conn syndrome
Primary hyperaldosteronism
```
Bilateral hyperplasia (more common)
Unilateral tumor
```
96
When to be suspicious
Low K
| HTN
97
Lab testing for Conn synd (hyperaldosteronism)
1. Increased Aldosterone in plasma
2. Decreased Renin in plasma
3. Spontaneous Hypokalemia
98
Tx of Conn synd (hyperaldosteronism)
Unilateral tumor: remove
| Bilateral hyperplasia: Spironolactone
99
Addison's dz
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
Secondary and tertiary insuff
will not have any Aldo sx (Aldo is normal)
| No hyperpigmentation
101
Secondary
low ACTH
102
Tertiary
low CRH
103
Cause of Addisons (low everything)
Auto-immune destruction of Adrenal Cortex
104
Cause of Secondary and Tertiary insufficiency
Abrupt cessation of Exogenous steroids is most common cause of Secondary
105
Dx Adrenal Insufficiency
Serum morning Cortisol
| Cosyntropin ACTH Stimulation test - find out where defect is
106
Cosyntropin ACTH test
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
Tx Addisons
Short acting steroid (hydrocortisone)
Long acting (Dexamethasone, prednisone)
Mineralcorticoid (if need estrogen replacement)
Consider oral DHEA for women
108
Pheo
Classic triad:
HA
Sweating
Tachycardia
109
Pheo tumors are usually
BENIGN 90%
| usually arise from Adrenal Medulla
110
When to suspect pheo
Paroxysmal "attach"
Refractory/persistent HTN
Onset HTN <20 YO
Family hx of pheo
111
Dx of Pheo
Plasma metanephrines
24 hr urine: VMA
Clonidine suppression test
112
Pheo dx
After labs, CT scan of abdomen WITHOUT contrast
113
Tx of Pheo
A-blocker (Phenoxybenzamine) and B-blocker (Propranolol)
SURGERY is definitive
114
Adrenal incidentaloma
>1 cm
115
For all pts w/ adrenal incidentaloma
R/o Pheo and Cushing
116
Pt has Adrenal Incidentaloma and HTN
R/o primary Hyperaldosteronism "Conn Synd"
117
Pt has Adrenal Incidentaloma and primary CA
DO NOT BIOPSY if suspect pheo or known METs
118
Adrenal incidentaloma workup is negative, likely benign, and mass is <2 cm
repeat imaging at 6 months
Repeat Dexamethasone suppression test (cushing test) yearly x 4 years
119
If workup negative, likely benign, BUT mass is >2cm
Consider SURGERY
120
Type 1 DM prone to other Auto-immune disorders
Thyroid dz, Celiac, Pernicious Anemia
121
Clinical sx of Type 1
```
3 Ps
Weight loss
Nocturia
Blurry vision
DKA
Fatigue
Paresthesias
Infections- candida
```
122
Type 2 DM
Gradual onset
| Genetic PreD is higher
123
Progression of Type 2 DM
Peripheral insulin resistance --> Impaired glucose tolerance --> Overt diabetes --> Beta cell failure "burnout"
124
Clinical sx of Type 2
Asymptomatic, OR
```
Polyuria, polydipsia
Blurred vision
Acanthosis Nigricans
Chronic skin infection
Vulvovaginitis, Balanitis
```
125
Screening for DM
Anyone overweight by BMI: 25 or more (23 or more in Asians) with 1 or more risk factors
and
ALL pts 45+ YO
126
Fasting plasma glucose
>126 is DM
127
2 hr Oral Glucose Tol Test- OGTT
200+ is DM
128
A1C%
>6.5% is DM
129
Normal A1C
<5.7%
130
Random plasma glucose
>200 AND classic DM sx is diagnosable
131
To diagnose Acute onset Type 1 DM with sx of hyperglycemia,
Blood glucose should be used rather than A1C
132
Pre Diabetes
Fasting: 100-125
2 hr: 140-199
A1C: 5.7%-6.4%
133
Consider Metformin for Pre-diabetic ESP IF
BMI >35
age 60+ YO
Women w hx of Pregestational DM
134
ASCVD (3 parts)
Coronary Heart Dz
Cerebrovascular Dz
Peripheral Artery Dz
135
Tx for ASCVD
Lifestyle
BP management
Lipid management
Antiplatelet (ASA or Colopidogrel/Plavix)
136
Diabetic Nephropathy
AKA
"Diabetic Kidney Dz"
occurs in 20-40% of pts with DM
Related to chronic hyperglycemia
137
Diabetic Nephropathy "Diabetic Kidney Dz"
typically after 10 yrs in type 1, may be present at Dx in Type 2
138
Clinical sx of Diabetic nephropathy "Diabetic Kidney dz"
Albuminuria
Reduced eGFR
(absence of another cause for the kidney damage)
139
Clinical progression of Diabetic Kidney dz
Long standing DM: progressive Albuminuria >300, HTN, and decline in GFR
140
Screen for Diabetic Nephropathy
AT least ONCE/YR
Urinary ACR
2-3 specimens of UACR within 3-6 month period have to be abnormal before diagnosing
141
Screen for Diabetic Nephroparhy
after 5 years of Type 1
| immediately for Type 2
142
Tx for Diabetic Nephroparhy
ACE-I and ARBs
| Intense glycemic and BP control
143
Diabetic Retinopathy
Highly specific vascular complication with Type 1 and 2
leading cause of blindness b/w age 20-74 in the US
144
Prevalence of DM Retinopathy related to
Duration AND level of glycemic control
145
Other Risk Factors for Diabetic Retinopathy
Nephropathy
HTN
Dyslipidemia
146
Two types of Diabetic Retinopathy
Non-prolif and Prolif
147
Non-proliferative DM Retinopathy
"Cotton wool spots"
Retinal hemorrhage
yellow lipid exudate
148
Proliferative DM
NEW VASCULATURE
| neovascularization
149
Clinical sx of Diabetic Retinopathy
often NONE until late dz
Refer to Ophtho!!!
150
Screening for DM Retinopathy
Type 1: within 5 yrs of dx
| Type 2: immediately
151
Diabetic Retinopathy after screening
If no sx for at least 1 annual exam and sugars well controlled, can then screen every 1-2 years
152
If any level of Diabetic Retinopathy is present
Sequental dilated retinal exam AT LEAST ANNUALLY
153
Diabetic Neuropathy
Peripheral vs Autonomic
154
Peripheral Neuroparhy
"Stocking glove"
Pain, numbness, LOPS (loss of protective sensation) Risk for ulcers
Loss of vibratory, proprioception
Decreased or absent ankle reflexes
155
Foot ulcers Risk Factors
```
Hx of ulcer
LOPS
Foot deformity: Charcot foot
PAD
Poor glycemic control
Callus or corn
CKD (esp on dialysis)
```
156
Comprehensive foot exam
```
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
ABI
ankle brachial index
158
Autonomic Neuropathy
```
Hypoglycemia unawareness***
Orthostatic hypotension
Gastroparesis***
Sexual dysfx
Incontinence
Diarrhea/constipation
Anhidrosis- sweating issues
Abnormal pupillary response
```
159
Referrals for DM
```
Eye
Family planning
Dietician
Diabetes self management
Dentist
Podiatrist
Mental health professional
```
