Clin Med Flashcards
Overweight
BMI 25-29.9
Obese
BMI 30+
BMI
weight (kg) / height (m^2)
When to measure waist circumference?
If BMI b/w 25-35
Increased cardiometabolic risk based on Weight circumference
M: 40+ inches
F: 35+ inches
Increased cardiometabolic risk based on Weight circumference (Asian)
M: 35.4+ inches
F: 31.5+ inches
As people lose weight
metabolism tends to slow down, making it harder to continue losing weight
How to lose weight by creating negative energy balance
Crease 500-1000 calorie per day deficit= 1-2 lbs of weight loss per week
Goals of weight loss
Initial goal:
5-7% of body weight
loss of >5% reduces risk factors for CVD
Commonly rec diets for weight loss and protection against DM and CAD
Mediterannean: low meat, fat is from olive oil, plant based
DASH (to stop HTN): veggies, fruit, low fat dairy, whole grains, fish, poultry, buts
Recommended for all of the following: Type 2 DM, CVD, Kidney dz
DASH
Intermittent fasting
Promote weight loss
Improves lipids
Reduces BP, fasting BS, and A1C
Obesity screening
Screen ALL Adults
if BMI 30+: refer for intensive, multicomponent behavioral intervention
If diagnosed obese, what is considered comprehensive and high intensity intervention?
2x/month for at least 3 months
12-26 sessions/year
The most important factor in a lifestyle change plan
Readiness to change
Low risk
BMI 25-29.9 with NO CVD, Risk factors, or other comorbidities
Tx: diet/exercise counseling
Moderate risk
BMI 25-29.9 AND 1 or more Risk factor
OR
BMI 30-34.9
Tx: intensive, multicomponent behavior modification + drug therapy for SOME
High risk
BMI 35-40
Intensive, multicomponent behavior modification + consider drug therapy or Surgery
Very high risk
BMI >40
Intensive, multicomponent behavior therapy + consider drug therapy or Surgery
When to consider meds for Obesity
BMI 30+ or >27 with comorbidity
When to consider meds for Obesity
AFTER 3-6 months, if <5% weight loss has been achieved
Goals of drug therapy
reduce weight by 4-8% within 6-12 months
Orlistat (Alli/Xenical)
Inhibit pancreatic lipase, altering fat digestion
Fatty stools, Unpleasant GI SE
Take Vitamin!! (may decrease absorption of fat soluble vitamins, ADEK)
Liraglutide (Victoza)
GLP-1 RA
(also a DM drug, Type 2)
Daily SQ injection
Phentermine/ Topiramate
DO NOT USE in pts with HTN, CAD, or Hyperthyroid
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
Bariatric surgery
Efficient, improve DM and HTN, lower long term mortality rates
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
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
CONTRA-indications to bariatric surgery
Eating disorder Untreated mental illness Drug/Alc abuse Coagulopathy Severe cardiac dz Cannot comply w new diet
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)
Exercise recommendation
aerobic
150-300 min of MODERATE
OR
75-150 min of VIGOROUS
Exercise recommendation
muscle strengthening
2 or more days/week
Hormones released from Ant Pit (6)
ACTH TSH LH FSH GH Prolactin
Ant Pit
Makes AND Secretes hormones in response to negative fdback from Adrenal, Thyroid, and Gonads
ACTH
stimulates production and release of Cortisol
LH in females
Triggers ovulation (LH Surge) and development of Corpus Luteum
LH in males
Tells Leydig cells to produce Testosterone
FSH in females
Growth of ovarian follicles
FSH in males
formation of Secondary spermatocytes
Prolactin in males
Work with LH and Testosterone to increase reproductive function
Posterior pit
ONLY RELEASES hormones that are made in hypothalamus
Intermediate pituitary
AKA
“Pars Intermedia”
MAKES and SECRETES Melanocyte stimulating hormone- skin pigmentation
ACTH made by
Corticotrophs
TSH made by
Thyrotrophs
LH and FSH made by
Gonadotrophs
GH made by
Somatotrophs
Prolactin made by
Lactotrophs
Sellar Mass clinical sx
Visual, diplopia, HA
Incidental finding on MRI
Why does visual change occur w Sellar mass?
Suprasellar extension of adenoma compressing the Optic Chaism
“Bitemporal hemianopsia”
AKA tunnel vision
Type of Sellar mass: Benign Tumor
Pituitary adenoma is a type of BENIGN
Most common Pituitary adenoma (a benign Sellar mass)
Prolactinoma
Clinical sx of Prolactinoma in pre-menopausal women
No period
Infertile
Galactorrhea
Serum prolactin level: >30
Clinical sx of Prolactinoma in post-menopausal women
HA
Impaired vision
Galactorrhea
Serum prolactin level >20
Clinical sx of Prolactinoma in Men
Decreased libido
ED, infertile
Gyencomastea
Serum prolactin level >20
Tx of Prolactinoma
Cabergoline (pharm)
OR
Transsphenoidal resection (standard of care)
GH excess most common cause
Benign pituitary macroadenoma (from somatotrophs)
Acromegaly
ADULTS
Increased risk of DM, HTN, and CAD
Growth Hormone Excess Dx
OGTT: >1 after two hours
GOLD STANDARD
Can also do IGF-1 levels, MRI
Tx of GH excess
Transsphenoidal Microsurgery: most successful in pts iwth GH <50 and tumor <2cm
Pharm: Somatostatin analog (Octreotide/lanreotide)
Monitoring of GH excess
IGF-1 levels every 3-6 months
GH deficiency (not enough)
Pit adenoma or after tx of tumor (removed too much)
Rare: Sheehan synd
GH deficiency in adults
Tumors are #1 cause
Tx of GH deficiency in adults
Only warranted if they have hx of childhood onset GH deficiency
Tx: daily injections of GH
Primary Hypogonadism
Hyper Hypo
problem with testis
Low testosterone
High FSH and LH
Secondary hypogonadism
Hypo Hypo
problem with Ant Pit
Low testosterone
Low/norm FSH and LH
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
If diagnosed Secondary Hypo (Hypo hypo),
test all other Ant pit hormones to make sure the entire Ant Pit is not broken
Tx for Hypo Hypo
IM injections every 2 wks
Transdermal cream/gel/patch daily
Pellets every 3 months
Hypo Hypo management
B4 tx: Rectal exam and PSA
Monitoring: Free and total T, CBC, Free Estradiol, Annual rectal and PSA
CONTRA to treating Hypo Hypo with testosterone
Hx of Prostate CA
Pan-Hypopituitarism
ENTIRE Ant Pit is not fx correctly, causing decrease of all hormones
Etiology: radiation (50%), tumor, Sheehan synd (rare)
Sheehan synd
Postpartum necrosis of Ant Pit d/t blood loss or shock
Most common initial sx of Sheehan
Agalactorrhea/ difficulties with breastfeeding
Dx of Sheehan syn
Hx and PE
Full hormone workup
MRI brain
Stimulation test
Tx of Sheehan
Extensive hormone replacement
Levothyroxine- thyroid, Dexamethasone- cortisol, T, Estrogen, GH, Ca and Vit D
Central Diabetes Insipidus
not enough ADH
- a lot of dilute urine
- thirsty
- nocturia/enuresis
SIADH
too much ADH
-little urine, very concentrated
Tx of Central Diabetes Insipidus
Desmopressin
available intranasally
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
Tx of SIADH
fluid restriction
Low dose Dexamethasone suppression test
Cushing synd
Cosynotropin (synthetic ACTH) Stimulation test
Addison’s dz
Clonidine suppression test
Pheochromocytoma
Aldosterone is regulated by
AT II
Serum K
ACTH
Cortisol
glucose regulation
Cushing synd (too much cortisol)
Stria Hyperpigmentation Moon face Buffalo hump HTN Osteroporosis Depression/Anxiety Amenorrhea Hirsuitism, Acne, increased libido
Cushing DISEASE
Pituitary hypersecretion of ACTH (very common, 70% of all Cushings syndrome)
ACTH dependent (more common, 80% of all cushings)
ACTH is HIGH
Female to male 8:1
ACTH independent
often from steroid use
pheochromocytoma
Diagnosing Cushing
- 24 hr urine free Cortisol (GOLD STANDARD)
1. then, Low dose dexamethasone suppression test
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
Pharm tx for Cushing
1st line: Ketoconazole
If Ketoconazole is not enough for Cushing dz
Add Metyrapone
Conn syndrome
Primary hyperaldosteronism
Bilateral hyperplasia (more common) Unilateral tumor
When to be suspicious
Low K
HTN
Lab testing for Conn synd (hyperaldosteronism)
- Increased Aldosterone in plasma
- Decreased Renin in plasma
- Spontaneous Hypokalemia
Tx of Conn synd (hyperaldosteronism)
Unilateral tumor: remove
Bilateral hyperplasia: Spironolactone
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
Secondary and tertiary insuff
will not have any Aldo sx (Aldo is normal)
No hyperpigmentation
Secondary
low ACTH
Tertiary
low CRH
Cause of Addisons (low everything)
Auto-immune destruction of Adrenal Cortex
Cause of Secondary and Tertiary insufficiency
Abrupt cessation of Exogenous steroids is most common cause of Secondary
Dx Adrenal Insufficiency
Serum morning Cortisol
Cosyntropin ACTH Stimulation test - find out where defect is
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
Tx Addisons
Short acting steroid (hydrocortisone)
Long acting (Dexamethasone, prednisone)
Mineralcorticoid (if need estrogen replacement)
Consider oral DHEA for women
Pheo
Classic triad:
HA
Sweating
Tachycardia
Pheo tumors are usually
BENIGN 90%
usually arise from Adrenal Medulla
When to suspect pheo
Paroxysmal “attach”
Refractory/persistent HTN
Onset HTN <20 YO
Family hx of pheo
Dx of Pheo
Plasma metanephrines
24 hr urine: VMA
Clonidine suppression test
Pheo dx
After labs, CT scan of abdomen WITHOUT contrast
Tx of Pheo
A-blocker (Phenoxybenzamine) and B-blocker (Propranolol)
SURGERY is definitive
Adrenal incidentaloma
> 1 cm
For all pts w/ adrenal incidentaloma
R/o Pheo and Cushing
Pt has Adrenal Incidentaloma and HTN
R/o primary Hyperaldosteronism “Conn Synd”
Pt has Adrenal Incidentaloma and primary CA
DO NOT BIOPSY if suspect pheo or known METs
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
If workup negative, likely benign, BUT mass is >2cm
Consider SURGERY
Type 1 DM prone to other Auto-immune disorders
Thyroid dz, Celiac, Pernicious Anemia
Clinical sx of Type 1
3 Ps Weight loss Nocturia Blurry vision DKA Fatigue Paresthesias Infections- candida
Type 2 DM
Gradual onset
Genetic PreD is higher
Progression of Type 2 DM
Peripheral insulin resistance –> Impaired glucose tolerance –> Overt diabetes –> Beta cell failure “burnout”
Clinical sx of Type 2
Asymptomatic, OR
Polyuria, polydipsia Blurred vision Acanthosis Nigricans Chronic skin infection Vulvovaginitis, Balanitis
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
Fasting plasma glucose
> 126 is DM
2 hr Oral Glucose Tol Test- OGTT
200+ is DM
A1C%
> 6.5% is DM
Normal A1C
<5.7%
Random plasma glucose
> 200 AND classic DM sx is diagnosable
To diagnose Acute onset Type 1 DM with sx of hyperglycemia,
Blood glucose should be used rather than A1C
Pre Diabetes
Fasting: 100-125
2 hr: 140-199
A1C: 5.7%-6.4%
Consider Metformin for Pre-diabetic ESP IF
BMI >35
age 60+ YO
Women w hx of Pregestational DM
ASCVD (3 parts)
Coronary Heart Dz
Cerebrovascular Dz
Peripheral Artery Dz
Tx for ASCVD
Lifestyle
BP management
Lipid management
Antiplatelet (ASA or Colopidogrel/Plavix)
Diabetic Nephropathy
AKA
“Diabetic Kidney Dz”
occurs in 20-40% of pts with DM
Related to chronic hyperglycemia
Diabetic Nephropathy “Diabetic Kidney Dz”
typically after 10 yrs in type 1, may be present at Dx in Type 2
Clinical sx of Diabetic nephropathy “Diabetic Kidney dz”
Albuminuria
Reduced eGFR
(absence of another cause for the kidney damage)
Clinical progression of Diabetic Kidney dz
Long standing DM: progressive Albuminuria >300, HTN, and decline in GFR
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
Screen for Diabetic Nephroparhy
after 5 years of Type 1
immediately for Type 2
Tx for Diabetic Nephroparhy
ACE-I and ARBs
Intense glycemic and BP control
Diabetic Retinopathy
Highly specific vascular complication with Type 1 and 2
leading cause of blindness b/w age 20-74 in the US
Prevalence of DM Retinopathy related to
Duration AND level of glycemic control
Other Risk Factors for Diabetic Retinopathy
Nephropathy
HTN
Dyslipidemia
Two types of Diabetic Retinopathy
Non-prolif and Prolif
Non-proliferative DM Retinopathy
“Cotton wool spots”
Retinal hemorrhage
yellow lipid exudate
Proliferative DM
NEW VASCULATURE
neovascularization
Clinical sx of Diabetic Retinopathy
often NONE until late dz
Refer to Ophtho!!!
Screening for DM Retinopathy
Type 1: within 5 yrs of dx
Type 2: immediately
Diabetic Retinopathy after screening
If no sx for at least 1 annual exam and sugars well controlled, can then screen every 1-2 years
If any level of Diabetic Retinopathy is present
Sequental dilated retinal exam AT LEAST ANNUALLY
Diabetic Neuropathy
Peripheral vs Autonomic
Peripheral Neuroparhy
“Stocking glove”
Pain, numbness, LOPS (loss of protective sensation) Risk for ulcers
Loss of vibratory, proprioception
Decreased or absent ankle reflexes
Foot ulcers Risk Factors
Hx of ulcer LOPS Foot deformity: Charcot foot PAD Poor glycemic control Callus or corn CKD (esp on dialysis)
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
ABI
ankle brachial index
Autonomic Neuropathy
Hypoglycemia unawareness*** Orthostatic hypotension Gastroparesis*** Sexual dysfx Incontinence Diarrhea/constipation Anhidrosis- sweating issues Abnormal pupillary response
Referrals for DM
Eye Family planning Dietician Diabetes self management Dentist Podiatrist Mental health professional
