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Medi Flashcards

1
Q

Masked Hypertension

A
  • No Hypertension
    • Office/Clinic
  • Hypertension
    • Home/ABPM Setting
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2
Q

Indications for ABPM

A
  1. Suspected White Coat Hypertension
  2. Suspected Episodic Hypertension
  3. Hypertension Resistant to Increasing Medication
  4. Hypotensive Symptoms when taking Antihypertensive Medication
  5. Determining Blood Pressure Control in Patients known to have substantial white coat effect
  6. Autonomic Dysfunction
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3
Q

HBPM

A

Self-recorded BP measurement taken at home or work

Better predictor of CVD risk due to elevated BP

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4
Q

ABPM

A

Device that takes BP measurements over a 24-48 hour period, usually every 15-20 mins during daytime and every 30-60 mins during sleep

Better predictors of CVD risk due to elevated BP

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5
Q

Hypertension Risk Factors

A
  1. Age
  2. Obesity
  3. Family Hx
  4. Race (More common and sever in African-Americans)
  5. High Sodium Diet
  6. Excess Alcohol Intake
  7. Physical Inactivity
  8. Secondary Causes
    1. Medications
    2. Contraceptives
    3. NSAIDs
    4. Decongestants
    5. Antidepressants
    6. Corticosteroids
    7. Stimulants
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6
Q

Complications of Hypertension

A
  1. Premature Cardiovascular Disease
  2. Heart Failure
  3. Left Ventricular Hypertrophy
  4. Ischemic Stroke
  5. Intracerebral Hemorrhage
  6. Chronic Kidney Disease (CKD) and End-Stage Renal Disease
  7. Life-Threatening Emergency
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7
Q

Diagnosis of Hypertension

A
  1. Accurately measure patient’s blood pressure
  2. Perform focused medical history and physical examination
  3. Obtain results of routine lab studies
  4. Testing
    1. 12-Lead EKG
    2. Consider CXR
  5. 10 Year CVD Risk or History of ASCVD
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8
Q

What should consist of a good history w/ hypertension?

A
  1. Medications (Including OTC)
  2. Past Med Hx
  3. Social Hx
  4. Family Hx
  5. Weight Changes
  6. Dietary Intake of Sodium and Cholesterol
  7. Exercise Level
  8. Psychosocial Stressors
  9. Other Symptoms
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9
Q

What should a physical exam for hypertension consist of?

A
  1. Fundoscopic eval of eyes
    1. Papilledema/hemorrhages
  2. Palpation of ALL Peripheral Pulses
  3. Thyroid Exam
  4. Cardiac Examination
    1. Murmurs/Extra Heart Sounds
  5. Listen to Lungs
  6. Listen for Renal Artery Bruits
  7. Extremities
  8. Skin Inspection
  9. Neurological Exam
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10
Q

Lab Testing/Diagnostics Hypertension

A
  1. Fasting Blood Glucose
  2. CBC
  3. Urinalysis
  4. Renal Fx: Creatinine
  5. BMP or CMP
  6. Lipid Profile
  7. TSH/FT4
  8. EKG
  9. Other
    1. Uric Acid, Echocardiogram, Urine Albumin/Cr Ratio
  • Obtain Urine Albumin/Cr Ratio in all patients w/ diabetes or chronic kidney disease
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11
Q

Lifestyle Modifications for Treatment of HTN

A
  • Weight Reduction
  • Sodium Reduction (<1500 mg/day)
  • Healthy Diet (DASH Diet)
  • Increase Physical Activity (120-150 min/wk)
  • Limited Alcohol Consumption
    • Men less than or equal to 2 drinks/d
    • Women less than or equal to 1 drink/d
  • Avoidance of Cigarette Smoking
  • Increase Dietary Potassium (3500-5000 mg/d)
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12
Q

Mechanism of Hypertension

A

BP = Cardiac Output x Systemic Vascular Resistance

Renin-Angiotensin-Aldosterone System

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13
Q

Medications for HTN

A
  • Thiazide Diuretics
  • Long-Acting Calcium Channel Blockers
  • ACE Inhibitors
  • Angiotensin II Receptor Blockers (ARBs)
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14
Q

Recommended treatment/follow-up for Normal BP

A
  • Promote Optimal Lifestyle Habits
  • Reassess in 1 Year
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15
Q

Recommended Treament/Follow-Up for Elevated BP (120-129/<80)

A
  • Nonpharmacologic Therapy
  • Reassess in 3-6 Months
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16
Q

Recommened Treatment/Follow-Up for Stage 1 HTN (130-139/80-89)

A
  • Clinical ASCVD or Estimated 10-y CVD Risk > or = 10%?
    • If Yes
      • Nonpharmacologic Therapy and BP-Lowering Med
      • Reassess in 1 Month
      • BP Goal Met?
        • Yes
          • Reassess in 3-6 Months
        • No
          • Assess and Optomize Adherence to Therapy
          • Consider Intensification of Therapy
          • Reassess in 1 Month
    • If No
      • Nonpharmacologic Therapy
      • Reassess in 3-6 Months
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17
Q

Recommened Treatment/Follow-Up for Stage 2 HTN (>140/90)

A
  • Nonpharmacologic Therapy and BP-Lowering Med
    • Reassess in 1 Month
    • BP Goal Met?
      • Yes
        • Reassess in 3-6 Months
      • No
        • Assess and Optomize Adherence to Therapy
        • Consider Intensification of Therapy
        • Reassess in 1 Month
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18
Q

What is the MOA for Thiazide Diuretics?

A

Inhibit reabsorption of sodium and chloride mostly in distal tubules

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19
Q

What is the MOA for CCB?

A

Promote vasodilation by reducing calcium influx into vascular smooth muscle cells by interfering w/ voltage-operated calcium channel

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20
Q

What is the MOA of ACE Inhibitors?

A

Prevent conversion of angiotensin I to angiotensin II

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21
Q

What is the MOA of ARBs?

A

Competitively block binding of angiotensin II to AT1 receptors, reducing effects of angiotensin II-induced vasoconstriction, sodium retention, and aldosterone release

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22
Q

What is the MOA for Beta-Blockers?

A

Antagonize effects of sympathetic nerve stimulation or circulating catecholamines at beta-adrenoceptors

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23
Q

What medication should be used with hypertension and diabetic nephropathy or nondiabetic chronic kidney disease w/ proteinuria?

A

ACE Inhibitor or ARB

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24
Q

What medication should be used for hypertension in African-Americans?

A

Thiazide Diuretic or Long-Acting Dihydropyridine CCB

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25
Q

Clinical Clue of Suggestive Secondary HTN

A
  • Severe or Resistant HTN
    • 3 Antihypertensive Agents and Not Controlled
  • Acute Rise in BP in a pt. w/ previously stable BP
  • Age <30 Years in Non-Obese
  • Malignant or Accelerated HTN
    • Severe HTN w/ Evidence of End-Organ Damage
  • Hypertension Associated w/ Electrolyte Disorders
    • Hypokalemia and Metabolic Alkalosis
  • Onset Before Puberty
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26
Q

Common Causes of Secondary HTN

A
  1. Renal Parenchymal Disease
  2. Renovascular Disease
  3. Primary Hyperaldosteronism
  4. Drugs/Alcohol
27
Q

Uncommon Causes of Secondary Hypertension

A
  • Pheochromocytoma
  • Cushing’s Syndrome
  • Hyper/Hypothyroidism
  • OSA
  • Coarctation of Aorta
  • Primary Hyperparathyroidism
28
Q

Hypertension w/ Elevated Serum Cr and/or Abnormal Urinalysis

A

Primary Kidney Disease

29
Q
  1. Suspicion of Secondary Hypertension
  2. Refractory or Malignant HTN
  3. Worsened Kidney Function During Treatment of HTN
    1. Especially w/ ACE Inhibitor or ARB
  4. Severe HTN and Diffuse Atherosclerosis
  5. Severe HTN and Unexplained Atrophic or Asymmetric Kidneys
  6. Severe HTN and Recurrent Episodes of Acute Pulmonary Edema or Refractory HF w/ Impaired Renal Function
    1. Lateralized Abdominal Bruit
A

Renal Artery Stenosis

30
Q

Diagnosis of Renovascular HTN

A
  • Tests
    • Duplex Doppler Ultrasonagraphy
    • CTA
    • MRA
  • Labs
    • Urinalysis
    • CBC
    • Serum Electrolytes (BMP, CMP)
    • BUN, Cr
31
Q

Treatment of Renovascular HTN

A
  • Lifestyle Modifications
  • Antihypertensive Medication
  • Surgery
32
Q

HTN w/ Hypokalemia

A

Primary Hyperaldosteronism

33
Q

When to test for primary aldosteronism

A
  • HTN and Hypokalemia
  • Severe or Resistant HTN
  • HTN and Adrenal Incidentaloma
  • HTN and Family Hx of Early-Onset HTN or Cerbrovascular Accident at Young Age
  • HTN and First-Degree Relatives w/ Documented Primary Aldosteronism
34
Q

Most Common Causes of Hyperaldosteronism

A
  1. Bilateral Adrenal Hyperplasia
  2. APAs - Aldosterone-Producing Adenoma
  • Symptoms/Signs
    • Muscle Weakness
    • Headaches
    • HTN
35
Q

Diagnosis of Primary Hyperaldosteronism

A
  • Plasma Aldosterone-Renin Ratio (PAC/PRA)
    • May need to verify w/ other confirmatory tests
  • Adrenal CT Scan in ALL pts. w/ PA
    • To determine subtype and exclude adrenal carcinoma
36
Q

How is PAC/PRA ratio measured?

A
  • Performed by ambulatory blood test in morning; random PAC and PRA (or PRC)
    • PRA and PRC normally undetectable in primary aldosteronism
    • PAC is >15 ng/dL
    • PAC/PRA ratio >20
  • Drugs that interfere w/ test
    • Mineralocorticoid Receptor Antagonist
      • Spironolactone and Diuretics Hold for 6 Weeks Before
    • ACEI and ARBs Increase PRC
      • Hold for 2 Weeks
37
Q

Treatment of Hyperaldosteronism

A
  • Normalize Serum Potassium
  • Normalize Blood Pressure
  • Consider Surgery
    • Unilateral Adrenalectomy
  • Spironolactone
38
Q

Signs and Symptoms of Sleep Apnea

A
  • Headache
  • Daytime Somnolence and Fatigue
  • Snoring
  • Difficulty in Concentration
  • Depression
  • Persistent Systemic Hypertension
  • Life-Threatening Cardiac Arrhythmias
39
Q

Diagnosis of Sleep Apnea

A
  • Polysomnogram (Sleep Study)
  • CPAP
40
Q

Resistant Paroxysmal HTN w/ headache, sweating, and palpitations

A

Pheochromocytoma

41
Q

Diagnosis of Pheochromocytoma

A
  • Plasma Free Metanephrines or Urinary Fractionated Metanephrines
    • Further metabolizedf to vanillylmandelic acid (VMA)
42
Q

Treatment of Pheochromocytoma

A
  • Surgical Removal = Treatment of Choice
  • Pre-Op:
    • Treat HTN and Volume Contraction
    • Alpha blockade to control HTN for 2 weeks prior to Beta Blockade to treat tachycardia
      • CCB may be used if beta blocker not tolerated
43
Q

What are the two main mechanisms of metabolic acidosis?

A
  1. Extrarenal processes including increased acid production and accelerated extrarenal loss of HCO3-
  2. Primary defect in renal acidification w/ no increase in extrarenal H+ production
    1. Renal input of new HCO3 is insufficient to regenerate HCO3 lost in buffering acid as in distal RTA; or filtered HCO3 is wasted as in proximal RTA
    2. Cl reabsorbtion is increased resulting in a hyperchloremic metabolic acidosis
44
Q

Anion Gap Acidosis

A

Contributed if accumulating acid contains an anion other than chloride

45
Q

Most common cause of increased anion gap

A

Metabolic Acidosis

46
Q

Normal Anion Gap

A

Normal is 12 (9-13 for Phys) or 3x Albumin

  • Most of unmeasured anion is albumin
47
Q

Anion Gap Acidosis Causes

A
  • Uremia
  • L-Lactic Acidosis (Type A)
  • D-Lactic Acidosis (Type B)
  • Alcoholic & Diabetic Ketoacidosis
  • Ethylene Glycol
  • Methanol
  • Toluene
48
Q

Anion Gap Acidosis

Gap >30 mEq/L

A

Most common anions are lactate (Lactic Acidosis)

B-hydroxybutyrate and acetoacetate (Ketoacidosis)

49
Q

Causes of High Anion Gap

A
  1. Metabolic Acidosis
  2. Lab Error
  3. Severe Volume Depletion (Hyeperalbuminemia)
  4. Respiratory Alkalosis
  5. Metabolic Alkalosis
  6. Severe Hyperphosphatemia
  7. Increase Anionic Paraproteins (IgA Myeloma)
50
Q

Type A (L-Lactic Acidosis)

A
  • Due to hypoxia
    • Tissue Hypo-perfusion (cardiac failure)
    • COPD
    • Severe Anemia
    • Carbon Monoxide
51
Q

Type B (D-Lactic Acidosis)

A
  • Liver and Renal Failure
  • Cancer
  • Exercise
  • Seizure
  • Thiamine Deficiency
  • Metformin
  • Alcohol in Malnourished
52
Q

Causes of Low/Negative Anion Gap

A
  • Lab Error - Most Common
  • Hypoalbuminemia - 2nd Most Common
  • Mono or Polyclonal Gammopathy
  • Bromide, Lithium, Iodide
  • Hypercalcemia and Hypermagnesemia
  • Low Na w/ SIADH
53
Q
  • Normal Anion Gap
  • Low Plasma K
  • Low Urine Anion Gap
  • Low Urine pH
  • Urine PCO2 >70
  • FEHCO3 >15%
  • High Urine Citrate
  • High TTKG
A

Proximal (Type 2 RTA)

54
Q
  • Normal Anion Gap
  • Low Plasma K
  • Low Urine Anion Gap
  • High Urine pH
  • Urine PCO2 <40
  • FEHCO3 5-10%
  • Low Urine Citrate
  • High TTKG
A

Distal RTA (Type 1 RTA)

55
Q
  • Normal Anion Gap
  • High Plasma K
  • Very Low Urine Anion Gap
  • Low to High Urine pH
  • Urine PCO2 <40
  • FEHCO3 10-15%
  • Low Urine Citrate
  • Low TTKG
A

Generalized Distal Defect RTA (Type 4 RTA)

56
Q
  • Normal Anion Gap
  • Low Plasma K
  • High Urine Anion Gap
  • Low or High Urine pH
  • Urine PCO2 >70
  • FEHCO3 <5%
  • Normal Urine Citrate
  • Low TTKG
A

Extrarenal HCO3 Loss

57
Q

What distinguishes extrarenal and renal causes of metabolic acidosis?

A

Urinary Anion Gap

UAG = (UNa + UK) - UCl

Normally is postive 30-50

58
Q

What does a negative urinary anion gap value suggest?

A

Increased renal excretion of unmeasured cation such as NH4

(Metabolic Acidosis of Extrarenal Origin is associated w/ increased NH4)

(Acidosis of renal origin is associated w/ positive UAG)

59
Q

Acute Metabolic Acidosis Shifts the Oxyhemoglobin Curve Which Direction?

A
  • Right
    • Faciliates O2 Delivery
    • Within a few hours, curve shifts to left
60
Q

Systemic Effects of Metabolic Acidosis

A
  • Respiratory
    • Kussmaul Respirations
    • Rapid Response & Complete in 12-24 Hours
  • Cardiac
    • Depressed contractility
    • Vasodilation & Decreased Vascular Resistance
  • CNS
    • Little in terms of mental status changes
  • Bone
    • Acute Acidosis - Bone Loss
    • Chronic Acidosis - Increased bone dissolution and calcium egress to ECF
  • Electrolytes
    • Mineral Acid-Induced = Increases K+
    • Organic Acid-Induced = No change K
    • Increases fraction of ionized calcium → Hypercalcuria
61
Q

True or False

Metabolic Alkolosis Inhibits Respiration.

62
Q

In Metabolic Alkalosis, how much does pCO2 increase for each 1 mmol/L increase in serum bicarb?

63
Q

Clinical Manifestations of Metabolic Alkalosis

A
  1. Hypokalemia
  2. Hypoxemia due to Hypoventilation
  3. Weakness
  4. Neurological Symptoms
    1. Seizures
    2. Tetany
    3. Delirium
    4. Stupor

CR III (4 decks)

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