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LMCC > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Etiology of hypoglycaemia can be defined into two broad categories?

A
  1. Insulin-mediated

2. Insulin Independent

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2
Q

Ddx for insulin-mediated hypoglycaemia?

A
  • Exogenous administration of insulin
  • Insulin secretagogue use
  • Insulin-secreting tumors (insulinomas, nesidioblastosis)
  • Post-bariatric surgery hypoglycemia
  • Insulin autoimmune hypoglycemia
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3
Q

What is an insulinomas

A

Insulinoma is a rare neuroendocrine tumor of insulin producing beta cells

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4
Q

What is an nesidioblastosis?

A

Nesidioblastosis is hypertrophy of insulin-producing beta cells in the pancreas.

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5
Q

Ddx for insulin independent hypoglycaemia?

A
  • Malnutrition or starvation
  • Cirrhosis/Hepatic Failure
  • Sepsis
  • End-stage renal disease
  • Advanced heart failure
  • Adrenal insufficiency
  • Hormone deficiency (cortisol, glucagon and epinephrine in insulin-deficient DM)
  • Non-islet cell tumours (typically the result of mesenchymal tumour overproduction of IGF-II)
  • Inborn error of carbohydrate metabolism, glycogen storage disease, gluconeogenic enzyme
  • Alcohol
  • Drugs (e.g. quinine, indomethacin, gatifloxacin, lithium, ACE inhibitors, β-adrenergic receptor blockers)
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6
Q

How does pseudohypoglycemia occur?

A

Pseudohypoglycemia occurs when processing of blood specimens in untreated test tubes is delayed and cells, such as red blood cells and leukocytes (especially if increased, as in leukemia or polycythemia), consume glucose. Poor circulation to the digits can also cause erroneously low fingerstick glucose measurements.

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7
Q

What are the symptoms of hypoglycaemia?

A
  • Autonomic nervous system activity – palpitations, sweating, tachypnea, tachycardia
  • Neuroglycopenic symptoms – caused by decreased activity of CNS – dizziness, headache, clouding vision, mental dullness, fatigue, confusion, seizures
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8
Q

The surge in _______ in response to low plasma glucose typically occur first in hypoglycaemia

A

Autonomic activity

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9
Q

What is Whipple’s triad which suggest a patient’s symptoms are from hypoglycemia?

A
  1. serum glucose <4.0 mmol/L
  2. neuroglycopenic symptoms (confusion, sensation of warmth, weakness or fatigue, severe cognitive failure, seizure, coma)
  3. rapid relief provided by administration of glucose
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10
Q

Investigations of hypoglycaemia?

A

When the cause of hypoglycemia is not evident, screen for oral hypoglycemic agents and measure plasma glucose, serum ketones, insulin, pro-insulin, C-peptide, and insulin antibodies during a spontaneous hypoglycemic episode or a supervised fast of up to 72 h

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11
Q

What is C-Peptide?

A

A short peptide released into the circulation when proinsulin is cleaved to insulin

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12
Q

How can C-Peptide be used to distinguish between Exogenous and Endogenous source of hyperinsulinemia

A

o Increased = endogenous

o Decreased or normal = exogenous

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13
Q

Treatment for mild to moderate hypoglycemia (autonomic and neuroglycopenic symptoms)?

A

Rule of 15s:

  1. Ingestion 15g carbs (glucose tabs)
  2. Wait 15 mins - Check BG again
  3. If <4 repeat dose of carbs
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14
Q

Treatment for severe (unconscious) hypoglycemia?

A

Glucagon 1mg (IM or SC) or 1 amp D50W IV

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15
Q

After initial management of hypoglycaemia what are the next steps?

A
  1. Get them a complex snack afterward

2. Reduce their insulin dose

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16
Q

What is hypoglycemic unawareness?

A

Patient remains asymptomatic until severely hypoglycemic levels are reached

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17
Q

Etiology of hyperglycemia?

A
  • Diabetes – impaired glucose tolerance, T1Dm, T2DM, gestational diabetes
  • Endocrinopathy - Cause peripheral insulin resistance like Cushing syndrome, acromegaly, and pheochromocytoma
  • Meds - corticosteroids, estrogen, beta blockers, epinephrine, thiazide diuretics, niacin, pentamidine
  • Destruction of the pancreas from chronic pancreatitis, hemochromatosis, pancreatic cancer, and cystic fibrosis
  • Total parental nutrition and dextrose infusion
  • Critical Illness/Physiologic Stress – acute pancreatitis, post-stroke, post MI, shock, stress hyperglycemia (trauma, surgery, burns)
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18
Q

What are the causes of hypoglycemic unawareness?

A
  • Decreased glucagon/epinephrine response
  • History of repeated hypoglycemia or low HbA1c
  • Autonomic neuropathy
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19
Q

What are the risk factors of hypoglycemic unawareness?

A

RFs: elderly, renal impairment, thin, missed meals, exercise, insulin, secretagogues

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20
Q

What is the treatment of hypoglycemic unawareness?

A

Tx: Get them to higher BG levels (>12) so their thermostat can reset and therefore notice their lows

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21
Q

Physical exam for hyperglycemia?

A
  1. General – ABCs
    - Airway: GCS
    - Breathing – monitor for Kussmaul breathing (rapid and deep respiration), fruity acetone breath (DKA)
    - Circulation – postural BP and HR, assess JVP, mucous membranes, urine output and capillary BG
  2. DERM – hyperpigmentation of the skin (r/o Addison’s disease)
  3. ABDO: abdominal tenderness (DKA)
  4. NEURO
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22
Q

Investigations for hyperglycemia?

A

Investigations: urinalysis/urine ketones, TSH, troponin, ABG, plasma glucose, lytes, Cr, bicarb, beta-hydroxybutyrate, CBC, urine/blood culture, amylase/lipase, plasma osmolality
- CXR

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23
Q

Describe the pathophysiology of diabetic ketoacidosis.

A

Insulin deficiency causes the body to metabolize triglycerides and amino acids instead of glucose for energy. Serum levels of glycerol and free fatty acids rise because of unrestrained lipolysis, as does alanine because of muscle catabolism. Glycerol and alanine provide substrate for hepatic gluconeogenesis, which is stimulated by the excess of glucagon that accompanies insulin deficiency.

Glucagon also stimulates mitochondrial conversion of free fatty acids into ketones. Insulin normally blocks ketogenesis by inhibiting the transport of free fatty acid derivatives into the mitochondrial matrix, but ketogenesis proceeds in the absence of insulin. The major ketoacids produced, acetoacetic acid and beta-hydroxybutyric acid, are strong organic acids that create metabolic acidosis.

The increase H is exchanged for potassium and thus causes hyperkalemia and eventually excreted. The potassium stores inside the body will therefore run low.

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24
Q

Causes of diabetic ketoacidosis?

A

Causes: insulin omission, infarction (MI, CVA), iatrogenic (steroids), new Dx, infection (stress increases release of epinephrine which releases glucagon which will result in increased blood glucose, loss of glucose in the urine and loss of water and therefore dehydration. You will also need alternative energy – generation of ketone bodies – ketoacidosis.

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25
Q

Symptoms of diabetic ketoacidosis?

A

Sx: weight loss, nausea, vomiting, abdominal pain, dehydration, hypotension, tachycardia, LOC, polyuria, blurry vision, nocturia
• Kussmaul resp (deep/labored breathing in an attempt to reduce CO2 – reduce acidity).

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26
Q

Diagnostic criteria for diabetic ketoacidosis?

A

Plasma glucose hyperglycemia 14-35 mmol/L, ketones in either blood or urine, metabolic acidosis pH <7.3 ABG, serum bicarb <15 mmol/L, anion gap > 14 mmol/L

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27
Q

Describe the treatment orders for diabetic ketoacidosis?

A

Diet: NPO
Activity: Limit to bed rest until resolution
Vitals and Neuro vitals: Q1H for first 4 hours, then Q2-4H until resolution
IV fluids:
Determine hydration status:
- Hypovolemic Shock: NS at 1-2L/hr until stable
- Mild/moderate dehydration: NS 500cc x4hr then 250cc x2hr
- When BG 12-14 mM, switch to 0.45% NaCl + 5% dextrose @ 250 cc/hr
Insulin:
Potassium:
Bicarbonate:
Accurate ins/outs +/- foley catheter

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28
Q

If pH <7.0 in DKA, 44.6 mM of _____ in 200cc of sterile water and infuse at 200cc/hr Q2H until pH >7.0

A

Sodium bicarbonate

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29
Q

Describe the management of insulin in DKA

A

o Hyperglycemia is corrected by giving regular insulin 0.1 unit/kg IV bolus initially, followed by continuous IV infusion of 0.1 unit/kg/hour in 0.9% saline solution.
o Check BG hourly, if BG does not fall >3 mM in first hr, check hydration level and double insulin every hour until BG drops 3-4 mM per hour.
o When plasma glucose becomes < 11.1 mmol/L in adults, 5% dextrose should be added to IV fluids to reduce the risk of hypoglycemia. Insulin dosage can then be reduced to 0.02 to 0.05 unit/kg/hour and should be maintained until the anion gap has narrowed and blood and urine are consistently negative for ketones.
o Insulin replacement may then be switched to regular insulin 5 to 10 units subcutaneously every 4 to 6 hours.
o When the patient is stable and able to eat, a typical split-mixed or basal-bolus insulin regimen is begun. IV insulin should be continued for 1 to 4 hours after the initial dose of subcutaneous insulin is given.

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30
Q

When can you determine that DKA is resolved?

A

BG <14mM, bicarbonate >15 mM, venous pH >7.3 and anion gap <12mM

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31
Q

Complications of DKA?

A

Complications: cerebral edema, acute respiratory distress, sepsis, MI, hypokalemia (Insulin causes K to shift from blood into cells, which can cause hypokalemia which can cause an arrhythmia)→ arrhythmia, hypoglycemia, mortality 1-2%

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32
Q

Describe the management of potassium in DKA

A

o Hyperkalemia b/c acidosis drives potassium out of cells initially, but the glucose causes diuresis which causes potassium to be excreted in urine and insulin treatment causes K into cells
o Hypokalemia prevention requires replacement of 20 to 30 mEq (20 to 30 mmol) potassium in each liter of IV fluid to keep serum potassium between 4 and 5 mEq/L (4 and 5 mmol/L).
o If serum potassium is < 3.3 mEq/L (3.3 mmol/L), insulin should be withheld and potassium given at 40 mEq/hour until serum potassium is ≥ 3.3 mEq/L (≥ 3.3 mmol/L);
o If serum potassium is > 5 mEq/L (> 5 mmol/L), potassium supplementation can be withheld.

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33
Q

Definition of hyperosmolar hyperglycemic syndrome (HHS/HONK)?

A

Hyperglycemia, increased plasma osmolality, negative ketones

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34
Q

Describe the pathophysiology of hyperosmolar hyperglycemic syndrome (HHS/HONK).

A
  • It usually develops after a period of symptomatic hyperglycemia in which fluid intake is inadequate to prevent extreme dehydration due to the hyperglycemia-induced osmotic diuresis.
  • Serum ketones are not present because the amounts of insulin present in most patients with type 2 diabetes are adequate to suppress ketogenesis. Because symptoms of acidosis are not present, most patients endure a significantly longer period of osmotic dehydration before presentation, and thus plasma glucose (> 600 mg/dL [> 33.3 mmol/L]) and osmolality (> 320 mOsm/L) are typically much higher than in diabetic ketoacidosis.
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35
Q

Precipitating factors of hyperosmolar hyperglycemic syndrome (HHS/HONK).

A
  • Acute infections and other medical conditions
  • Drugs that impair glucose tolerance (glucocorticoids) or increase fluid loss (diuretics)
  • Nonadherence to diabetes treatment
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36
Q

Symptoms of hyperosmolar hyperglycemic syndrome (HHS/HONK)?

A

The primary symptom of hyperosmolar hyperglycemic state is altered consciousness varying from confusion or disorientation to coma, usually as a result of extreme dehydration with or without prerenal azotemia, hyperglycemia, and hyperosmolality.

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37
Q

Treatment for hyperosmolar hyperglycemic syndrome (HHS/HONK)?

A

• ABCs
• IV 0.9% saline - At a rate of 15 to 20 mL/kg/hour, for the first few hours. After that, the corrected sodium should be calculated. If the corrected sodium is < 135 mEq/L (< 135 mmol/L), then isotonic saline should be continued at a rate of 250 to 500 mL/hour. If the corrected sodium is normal or elevated, then 0.45% saline (half normal) should be used.
• Correction of any hypokalemia - similar to that in diabetic ketoacidosis: 40 mEq/hour for serum potassium < 3.3 mEq/L (< 3.3 mmol/L); 20 to 30 mEq/hour for serum potassium between 3.3 and 4.9 mEq/L (3.3 and 4.9 mmol/L); and none for serum potassium ≥ 5 mEq/L (≥ 5 mmol/L).
• IV insulin (as long as serum potassium is >3.3 mEq/L [>3.3 mmol/L])
o Safe to stop insulin drip after: long acting SC injection (0.2U/kg), 2 successful normal anion-gaps, and pt able to eat food by mouth

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38
Q

Definition of DM?

A

Diabetes mellitus is a heterogeneous metabolic disorder characterized by the presence of hyperglycemia due to impairment of insulin secretion, defective insulin action, or both

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39
Q

List the 4 ways to diagnosis DM?

A

o Fasting plasma glucose > 7.0 mmol/L OR
o HbA1C > 6.5% in adults OR
o 2h plasma glucose in 75g OGTT > 11.1 mmol/L OR
o Random plasma glucose > 11.1 mmol/L
o In the presence of hyperglycemia symptoms (polyuria, polydipsia, polyphagia, weight loss, blurry vision), a confirmatory test is not required
o In the absence of hyperglycemic symptoms, a repeat confirmatory test (FPG, A1C, 2h PG in a 75g OGTT) done on another day is required for diagnosis of diabetes

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40
Q

HbA1c for pre-diabetes?

A

A1c > 6.0%

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41
Q

What does HbA1c reflect?

A

Reflects glycemic control over 3 mo and is a measure of patient’s long-term glycemic control

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42
Q

What are the symptoms of diabetes?

A

Incidental finding of hyperglycemia (polydipsia, polyuria, nocturia, blurred vision, fatigue, poor concentration, recurrent infections (yeast), weight loss→ suggests insulin deficiency), osmotic Sx, medical emergency (DKA, Coma)

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43
Q

What should be done on physical exam for DM?

A

o Vitals: BP/orthostatic hypotension (diabetic autonomic neuropathy), HR/delayed postural HR response, RR. BP goal <130/80 mmHg
o Hands: Stiff hands + prayer signs (limited joint mobility or diabetic cheiroarthropathy), Dupuytren’s contracture. Assess for burning, paresthesias, sensory loss in the median nerve distribution, positive Tinel’s and Phalen’s test (carpal tunnel syndrome)
o Derm: Inspect for presence of infections
o HEENT: Acanthosis nigricans, JVP
o Eyes: Pupillary response to light, EOM, fundoscopy. Should see ophthalmology
o CV: palpation – assess for carotid and femoral artery bruits, peripheral artery pulses. Auscultate – ventricular dysfunction (diabetic cardiomyopathy)
o Feet: Assess for diabetic foot

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44
Q

What are the investigations for DM?

A

Lytes, CBC, UA, serum ketones, HCG (if F)

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45
Q

When is the typical onset of T1DM

A

Onset: Usually <30 yr of age

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46
Q

What percentage of cases of T1DM have no family Hx?

A

90% of cases no family Hx

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47
Q

T1DM is associated with which MHC class II cell surface receptor?

A

Associated with HLA-DR-DQ

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48
Q

Define T1DM

A

Beta cell destruction by lymphocytic infiltrates, typ. leading to absolute insulin deficiency, can be autoimmune or idiopathic

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49
Q

Target for T1DM

A

Target might be between 7.1-8.5% with limited life expectancy

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50
Q

Mainstay treatment for T1DM?

A

Insulin replacement

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51
Q

How do you calculate the total daily dose of insulin?

A

To calculate total daily dose is 0.3 unit per kg of body weight. (40-50% basal, 50-60% bolus – basal-bolus insulin therapy, more physiologic, bolus insulin often given with meals, promotes glucose utilization + uptake after meal, controls postprandial glucose)

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52
Q

What is Type 2 diabetes mellitus?

A

Peripheral insulin resistance +/or insulin deficiency

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53
Q

Typical onset for T2DM?

A

Usually >40 yr of age. Increasing incidence in pediatric population 2o to obesity

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54
Q

Risk factors for T2DM?

A

Risk factors: central obesity, sedentary lifestyle, family Hx, ethnicity (aboriginal, Hispanics, black), gestational diabetes, acanthosis nigricans

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55
Q

Initial management of T2DM with A1c <8.5%?

A

If initial A1c <8.5% → metformin or reassess 2-3mos. Initiate non-insulin antihyperglycemic therapy within 2-3m if lifestyle (diet, exercise, smoking cessation) does not result in glycemic control.

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56
Q

1st choice treatment option of T2DM

A

Metformin

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57
Q

Initial management of T2DM with HbA1c >8.5%?

A

If initial HbA1c >8.5% at time of diagnosis, initiate pharmacologic therapy with metformin immediately and consider combination of therapies

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58
Q

S/E of metformin?

A

Biggest S/E is diarrhea, anorexia, lactic acidosis

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59
Q

Absolute contraindications of metformin?

A

ABSOLUTE: Moderate to severe liver dysfunction. Moderate renal dysfunction GFR <30 mL/min. Cardiac dysfunction

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60
Q

What are the insulin secretagogues

A

Sulfonylureas, meglitinides

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61
Q

S/E of the insulin secretagogues?

A

S/E: Hypoglycemia. Weight gain.

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62
Q

Absolute contraindications of the insulin secretagogues?

A

Moderate to severe liver dysfunction

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63
Q

Interactions of the insulin secretagogues?

A

Do not combine with a non-sulfonylurea insulin secretagogue or preprandial insulin.

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64
Q

Benefit/advantage of metformin?

A

No hypoglycemia or weight loss, can combine with insulin

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65
Q

What are thiazolidinediones (TZDs)?

A

Insulin sensitizers

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66
Q

Benefit/advantage of thiazolidinediones (TZDs)?

A

No hypoglycemia risk

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67
Q

Absolute contraindications of thiazolidinediones (TZDs)?

A

NYHA > class II CHF

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68
Q

Interactions of thiazolidinediones (TZDs)?

A

Do not combine with insulin

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69
Q

Risk of SGLT-2 inhibitors?

A

Cause euglycemic DKA

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70
Q

Absolute contraindications of SGLT-2 inhibitors?

A

Severe renal impairment, ESRD, patients on dialysis

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71
Q

How do alpha glucose inhibitors work?

A

Acarbose: slows digestion of oligosaccharides→ monosaccharides, slows delivery of glucose to circulation

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72
Q

Biggest down side to alpha glucose inhibitors?

A

Poorly tolerated – diarrhea and gas

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73
Q

Target of BP with DM?

A

Target: <130/80

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74
Q

First-line therapy for type 1 and type 2 diabetic patients with microalbuminuria, even if they are normotensive?

A

ACEi or ARB

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75
Q

Target for LDL in patients with DM?

A

Target: LDL <2.0mmol/L

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76
Q

Which diabetic patients should be on a statin?

A

Statin therapy if >40yo OR macro/microvascular disease OR long duration of DM (>15 yrs and >30 y/o)

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77
Q

How to screen for CKD in diabetic patients

A

Screen with serum creatinine and random urine ACR + urinalysis

  • T1DM – exam 5 years post Dx and then annually
  • T2DM – exam at Dx and then annually
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78
Q

Target of ACR for diabetic patients

A

Target: Normal ACR <2.0 mg/mmol/L

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79
Q

How to screen for retinopathy in diabetic patients

A
  • Investigations: Direct ophthalmoscope - neovascularization or vitreous hemorrhage; macular edema
  • Follow-Up:
    • T1DM – exam 5 years post Dx and then annually
    • T2DM – exam at Dx and then 1-2 years if no retinopathy
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80
Q

What is autonomic neuropathy?

A

Resting tachycardia, postural hypotension, ED, abnormal sweating, gastroparesis, constipation/diarrhea

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81
Q

What is distal symmetrical sensory peripheral neuropathy?

A

Glove + stocking distribution, foot ulcers, amputations

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82
Q

S/S of neuropathic foot ulcers?

A

Plantar, pressure areas associated callus, painless, warm feet with dilated veins

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83
Q

S/S of ischemic foot ulcers?

A

Dorsum/lateral, painful, punched out, cold, pale, pulseless

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84
Q

What is Charcot foot?

A

Destruction of bony structure, consequence of neuropathy

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85
Q

Target for glycemic control in the hospital?

A

6-10 mmol/L is target for glycemic control

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86
Q

What test can you do to determine whether patient has T1DM or T2DM?

A

 A normal C-peptide range is 0.5 to 2.0 nanograms per milliliter.
 These levels can be high when your body makes more insulin than usual. Levels are low when your body makes less than it normally should.

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87
Q

Insulin complications

A

Weight gain, hypoglycemia, lipohypertrophy, lipoatrophy, insulin allergy

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88
Q

How to calculate insulin requirements in hospital?

A

• TIDM = Weight (kg) x 0.15-0.3 – Total Daily Dose
• T2DM = Weight (kg) x 0.3-0.5 – Total Daily Dose
• Then divide the TDD in half = basal 50%, bolus 50%.
o Bolus divide by 3 for peri prandial

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89
Q

Definition of short stature

A

Definition: height is 2 standard deviations (SD) or more below the mean for children of that sex and chronologic age

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90
Q

Etiology of short stature?

A 
ABCDEFG
	Alone (neglected infant)
	Bone dysplasias (rickets, scoliosis, mucopolysaccharidoses)
	Chromosomal (Turner, Down)
	Delayed growth (constitutional) 
	Endocrine (low GH, Cushing, hypothyroid) 
	Familial
	GI malabsorption (celiac, Crohn’s)
	IUGR
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91
Q

What distinguishes Familial Short Stature with Constitutional Delay of Growth?

A

Normal bone age - consistent with chronological age

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92
Q

Are pre-pubertal and pubertal growth velocities normal or abnormal in Familial Short Stature?

A

Normal pre-pubertal and pubertal growth velocity, short parents, normal timing of pubertal onset - final height within expected range without intervention

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93
Q

Are pre-pubertal and pubertal growth velocities normal or abnormal in Constitutional Delay of Growth/Puberty?

A

Normal pre-pubertal growth velocity but late onset of puberty.

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94
Q

What is the hallmark of Constitutional Delay of Growth/Puberty?

A

Delayed skeletal age; growth typically continues LONGER than normal, but results in adult stature within normal range

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95
Q

Should children with Constitutional Delay of Growth/Puberty achieve normal final height without intervention?

A

Yes

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96
Q

What is idiopathic short stature?

A

Height < 2 standard deviations below the mean for age with no identified pathology, normal growth velocity and bone age

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97
Q

What are the normal variants of growth for short stature?

A
  • Familial Short Stature
  • Constitutional Delay of Growth/Puberty
  • Idiopathic short stature
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98
Q

What are the pathologic causes for short stature?

A
  • Undernutrition
  • Glucocorticoid therapy
  • Chronic diseases: Celiac disease, GI disease, Rheumatologic disease (JIA), Chronic kidney disease
  • Endocrine: Achondroplasia, Cushing syndrome, Acquired GH deficiency, Congenital growth hormone deficiency, Hypothyroidism
  • Genetic disease: Turner syndrome, SHOX gene variants, Prader-Willi syndrome
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99
Q

What is the hallmark of undernutrition?

A

The hallmark of undernutrition is low weight-for-height.

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100
Q

What are the symptoms seen with Celiac disease?

A

Abdominal pain, malabsorption, anemia; short stature may be the only symptom

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101
Q

Children with growth failure resulting from gastrointestinal disease tend to have a greater deficit in _____ in contrast to those with endocrine disorders, who are often ______.

A

Children with growth failure resulting from gastrointestinal disease tend to have a greater deficit in weight than height (ie, they are underweight-for-height) in contrast to those with endocrine disorders, who are often overweight-for-height

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102
Q

Symptoms + signs of achondroplasia?

A

Short limbs; long, narrow trunk; large head with prominent forehead

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103
Q

Most common cause of Cushing syndrome?

A

The most common cause is a corticotropin (ACTH)-secreting pituitary adenoma (Cushing disease)

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104
Q

Best test to establish diagnosis of Cushing syndrome?

A

The best tests to establish the diagnosis are a 24-hour urine collection for free cortisol (and creatinine), or a dexamethasone suppression test

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105
Q

What risk factors would make you think acquired GH deficiency?

A

History of head trauma or cranial irradiation, central nervous system infection

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106
Q

Features of Turner syndrome?

A

Turner syndrome: Short stature, webbed neck, characteristic facies, short metacarpals, broad chest with widely spaced nipples, hyperconvex fingernails and toenails; may be normal appearing; decreased growth velocity and delayed puberty

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107
Q

Features of congenital growth hormone deficiency?

A

Hypoglycemia, birth length may be normal, height and bone age progressively delayed; jaundice, microphallus, midline craniofacial abnormalities

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108
Q

What should be obtained on history for short stature?

A

 Determine: onset of short stature, i.e. the need to change shoe/clothing sizes, relative height difference between peers and siblings + dietary history
 BIND History: prenatal history, delivery weight/length/GA, any IUGR/SGA/prematurity, neonatal hypoglycemia or prolonged jaundice, developmental history
 PMHx + Pubertal Onset Hx + Medications: corticosteroid or stimulant use
 FMHx: family members’ heights + pubertal history  calculate target height (mid parental height)
 ROS: for systemic diseases – GI, cardiac, renal, hypothyroid, neuro

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109
Q

Risk factors for GH deficiency?

A

Previous head trauma, history of intracranial bleed or infection, head surgery or irradiation, positive family history, breech delivery

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110
Q

What should be done on physical exam for short stature?

A
  • Calculate mid-parental height: children are usually in a percentile between their parents’ height
  • Tanner Staging: assess pubertal development
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111
Q

How do you calculate mid-parental height?

A

(mid-parental height = (mother + father’s height in cm ± 13cm)/2) - normal children should be within 10cm of this target

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112
Q

How do you confirm bone age for constitutional delay?

A

Confirm with bone age XR - AP x-ray of left hand and wrist for bone age

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113
Q

Investigations for short stature

A

CBC (anemia), CRP (IBD), Follicle-stimulating hormone, karyotyping (Turner), Insulinlike growth factor 1 (GH deficiency), TSH, free T4 (hypothyroidism, UA (renal disease), Tissue transglutaminase and total immunoglobulin A (celiac)

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114
Q

______ is approved for a variety of conditions that cause short stature, including Turner syndrome, chronic renal failure, Prader-Willi syndrome, small for gestational age, Noonan syndrome, short stature homeobox-containing gene deficiency, and idiopathic short stature.

A

Recombinant growth hormone

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115
Q

Definition for intrauterine growth restriction?

A

Definition: <10th%ile fetus that has not reached its growth potential. Infant weight <10%ile for GA or <2500g or abdominal circumference <10%ile.

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116
Q

What are the 3 types of IUGR?

A 
- Symmetric IUGR – Type 1
1A: constitutional (small women)
1B: intrinsic
- Asymmetric IUGR – Type 2
- Indeterminate IUGR – Type 3
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117
Q

What are the causes of symmetric IUGR - Type 1?

A

Congenital or TORCH

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118
Q

Is symmetric IUGR - Type 1 early or late gestational onset?

A

Growth inhibition early in gestation due to fetal abnormalities/insult. Inhibition of active mitosis, affecting cell hyperplasia.

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119
Q

What are the causes of asymmetric IUGR - Type 2?

A

Placental insufficiency (redistribution of blood to critical organs: brain, heart, adrenals preserved, brain sparing effect) or external factor – brain/heart/adrenals spared, ^MCA doppler =

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120
Q

What are the causes of indeterminate IUGR – Type 3?

A

Maternal vascular disease (lupus, HTN)

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121
Q

Does indeterminate IUGR – Type 3 affect cell hypertrophy or cell hyperplasia?

A

Decrease in cell hypertrophy and cell hyperplasia.

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122
Q

What is preserved in asymmetric IUGR - Type 2?

A

Asymmetric reduced weight for length. Preserved head size (brain sparing), abdomen small - loss of subcut fat, decreased muscle mass.

123
Q

Is symmetric IUGR - Type 2 early or late gestational onset?

A

Growth inhibition late in gestation affecting cell hypertrophy and growth, usually > 23 weeks! Later in pregnancy.

124
Q

Etiology for IUGR?

A

Due to maternal (nutrient delivery), placental (nutrient transfer), or fetal (nutrient utilization) factors

125
Q

Maternal factors for IUGR?

A

Maternal: nutrient delivery! Medical disorders affecting vascular/O2 system, nutrition issues, age, smoking/alcohol/substance.

126
Q

Placental factors for IUGR?

A

Placental: nutrient transfer! Placenta previa, chronic abruption, placental tumours, infarction, elevated maternal biochem, low PAPPA-A on FTS, confined placental mosaicism.

127
Q

Fetal factors for IUGR?

A

Fetal: nutrient utilization! Multiple gestation (why? inadequate placental reserve, occurs more in monozygotic), infection (5-10% of IUGR cases e.g. TORCH – toxo, other (varicella, syphilis), rubella, CMV, herpes), genetic disorders, congenital anomalies/malformations.

128
Q

Management of IUGR?

A

Management: basics, low dose Aspirin start at 12-16 weeks if at risk, LMWH, delivery near term - >37 weeks gestations

129
Q

What is used as a screening test for IUGR?

A

Fundal height (used as a screening test for all women after 20 weeks, >3cm lag - US

130
Q

Test that is diagnostic for IUGR?

131
Q

What is concerning on uterine artery doppler flow assessment?

A

Absent diastole or reflux means blood is leaving fetus and not going to mom or placental resistance is so high it comes back to baby

132
Q

Definition of tall stature?

A

Height greater than two SD above the mean for a given age, sex, and race

133
Q

Normal variants of tall stature?

A

Constitutional advancement of growth

Familial tall stature

134
Q

What is constitutional advancement of growth?

A

Refers to a growth pattern that is characterized by growth acceleration soon after birth, family history of early puberty, bone age greater than chronologic age

135
Q

What is familial tall stature?

A

Projected height within 5 cm (2 in) of midparental height, bone age greater than chronologic age, normal growth velocity after catch-up growth

136
Q

What are the endocrine disorders that can cause tall stature?

A
  • Hyperthyroidism:
  • Obesity: Body mass index greater than the 95th percentile
  • Pituitary gigantism (excess growth hormone)
  • Precocious puberty
137
Q

What is defined as precocious puberty in boys and girls?

A
  • Girls: breast development before 8 years of age

* Boys: testicular enlargement (> 3 mL) before 9 years of age

138
Q

Clinical features of pituitary gigantism?

A

Coarse facial features, mandibular prominence, broad root of nose, broad hands and feet, excessive sweating, hypertension, glucose intolerance

139
Q

Clinical features of hyperthyroidism?

A

Rapid childhood growth, goiter, tachycardia, hypertension, diarrhea, fine tremor, exophthalmos

140
Q

Investigations for tall stature?

A

Insulin like growth factor 1, Karyotyping (Klinefelter syndrome), Serum luteinizing hormone, follicle-stimulating hormone, testosterone (Precocious puberty), Thyroid-stimulating hormone, free thyroxine (T4) (Hyperthyroidism)

141
Q

Potential treatments for pituitary gigantism?

A

In patients with pituitary gigantism, octreotide (Sandostatin) and pegvisomant (Somavert) have been used to suppress the growth hormone

142
Q

What are the genetic causes of tall stature?

A
  • Klinefelter syndrome (XXY)

- Marfan syndrome

143
Q

Clinical features of Klinefelter syndrome (XXY)?

A

Delayed puberty; infertility; small, firm testes; gynecomastia; high-pitched voice; learning disability

144
Q

Clinical features of Marfan syndrome?

A

Increased arm span, thin extremities, superior subluxation of lens, hypotonia, kyphoscoliosis, cardiac valvular deformities, aortic root dilation

145
Q

What is the definition of polyuria

A

Polyuria has generally been defined as a urine output exceeding 3 L/day in adults and 2 L/m2 in children. It must be differentiated from the more common complaints of frequency or nocturia, which may not be associated with an increase in the total urine output

146
Q

What is water diuresis and the possible etiologies?

A

Absence or decreased secretion of ADH
o Excessive intake – primary polydipsia
o Excessive loss – (central & nephrogenic) diabetes insipidus

147
Q

What is osmotic diuresis and the possible etiologies?

A

Presence of large quantity of unabsorbed solute in renal tubules, inability to reabsorb a substantial proportion of the filtered solute
- Glucosuria - Hyperglycemia (DM), SGLT2 inhibitor use
- Urea - most often occurs in patients with resolving acute kidney injury
 Resolution from azotemia
 Exogenous administration of urea - therapy in patients with hyponatremia
 Tissue catabolism (eg, due to glucocorticoids) - Lean body tissues are approximately 20 percent protein by weight, and protein catabolism results in the production of urea.
- Sodium (eg, due to intravenous volume expansion)
- Mannitol (ie, given to patients with increased intracranial pressure)

148
Q

First step in the approach to polyuria?

A

Identify hyperglycemia or another obvious osmotic diuresis

  • Diabetic patients with severe hyperglycemia and glucosuria, SGLT2 inhibitor use, treatment with exogenous urea or glucocorticoids, administration of large volumes of saline, administration of mannitol
149
Q

When the etiology is not obvious for polyuria, how do you confirm the presence of polyuria?

A
  • Collect 24hr urine specimen – measure osmolality, creatinine, sodium, potassium, chloride, urea and glucose
  • Plasma lytes, glucose, Cr and BUN
150
Q

How can the osmolarity of urine help differentiate between osmotic diuresis or water diuresis?

A

<300 mOsm/L: water diuresis

> 300 mOsm/L

  • If over >600 mOsm/L: osmotic diuresis
  • Total daily osmolar output >1000 mOsm/L: osmotic diuresis, if not then water diuresis
151
Q

How can the specific gravity of urine help differentiate between osmotic diuresis or water diuresis?

A
  • Water diuresis: <1.010

- Osmotic diuresis: >1.010

152
Q

Pathophysiology of diabetes insipidus (DI)?

A

Lacking ADH, large volumes dilute urine, polydipsia, polyuria

153
Q

What are the types of diabetes insipidus (DI)?

A
  1. Central
  2. Nephrogenic diabetes insipidus
  3. Gestational
  4. Primary polydipsia
154
Q

What is central diabetes insipidus (DI) and possible causes?

A

Issue with the hypothalamus or pituitary gland preventing the release of ADH

This condition is most often idiopathic (possibly due to autoimmune injury to the ADH-producing cells) or can be induced by trauma, pituitary surgery, or hypoxic or ischemic encephalopathy

155
Q

What is nephrogenic diabetes insipidus (DI) and possible causes?

A

Nephrogenic diabetes insipidus (DI) is characterized by normal ADH secretion but varying degrees of renal resistance to its water-retaining effect
• Congenital (mutation of vasopressin receptor (V2) or mutation of the aquaporin gene)
• Acquired (lithium - reduced aquaporin channel, inhibits cAMP formation in collecting tubule)
• Hypercalcemia (downregulation of water channel in the medulla, tubulointerstitial damage from calcium deposit)

156
Q

What is gestational diabetes insipidus (DI)?

A

The placenta releases vasopressinase which breaks down vasopressin

157
Q

What is primary polydipsia and who is it most often seen in?

A

Primary polydipsia (sometimes called psychogenic polydipsia) is characterized by a primary increase in water intake. This disorder is most often seen in middle-aged women and in patients with psychiatric illnesses, including those taking a phenothiazine, which can lead to the sensation of a dry mouth

158
Q

Investigations:

A

Water Deprivation Test: Water deprived for eight hours.

  1. Weigh patient hourly (stop test if the patient loses 3-5% body weight)
  2. Serum and urine osmolality at beginning, hourly and end of test.
  3. Administer vasopressin, measure urine osmolality one hour later
159
Q

What would be seen on water deprivation test for central DI, nephrogenic DI and primary polydipsia?

A
  • Central DI - Uosm remains low after 8h but ↑ with vasopressin (DDAVP)
  • Nephrogenic DI - Uosm remains low after 8h and no increase with DDAVP
  • Primary polydipsia - Uosm ↑ after 8 h of dehydration
160
Q

What is the treatment for DI (central and nephrogenic)?

A

Desmopressin (central)

Thiazide diuretics – increase urine excretion of sodium (nephrogenic)

161
Q

What are the possible etiologies of weight gain?

A

Increased energy intake
 Dietary (e.g., progressive hyperphagic, frequent eating, high fat diet, overeating)
 Social and behavioral (e.g., socioeconomic, psychological)
 Iatrogenic (e.g., drugs, hormones, hypothalamic surgery)

Decreased energy expenditure (e.g., sedentary lifestyle, smoking cessation)
 Neuroendocrine (e.g., hypothyroidism, Cushing syndrome, polycystic ovarian syndrome)
 Genetic (e.g., Prader-Willi) - Heritability of BMI is about 66%
 Epigenetic

162
Q

What are the classifications of obesity in adults?

A

 Underweight <18.5
 Overweight BMI 25-29.9
 Obesity I 30-34.9, obesity II 35-39.9, obesity III >40

163
Q

What are the types of obesity in adults?

A

 Subcutaneous – pear. Less dangerous but harder to get rid of
 Visceral – apple Fat that accumulates around abdomen, pushes the abdomen out, the fat secretes a lot of inflammatory meditators that lead to other diseases

164
Q

What are the two main pathways regulating food intake?

A
  • Leptin: Hormone predominantly made by adipose cells that helps to regulate energy balance by inhibiting hunger. Obese patients have increased levels which implies they have a resistance to leptin (receptor/post-receptor defect). Receptors in hypothalamus, signals decreased food seeking + increased thermogenesis
  • Neuropeptide y (orexin): most potent stimulator of feeding, in obesity chronically elevated levels of NPY can be seen
165
Q

Low BMI associations?

A

Osteoporosis, eating disorders, undernutrition, pregnancy complications

166
Q

Adverse medical consequences of obesity?

A

T2DM, CAD, stroke, HTN, gallbladder disease, non-alcoholic steatohepatitis, pregnancy complications, dyslipidemia, osteoarthritis, sleep apnea, certain cancers, CHF, low back pain, ^total mortality

167
Q

Screening/assessing comorbidities for obesity?

A

BP + HR + FG + lipid profile + assess/screen for depression, eating/mood disorders + treat comorbidities and other risks, if present + assess readiness to change behaviours/barriers to weight loss

Use CANRISK or FINRISC scores to assess risk for T2DM in those who are overweight or obese

BMI risk assessment should be done every 3-5 years in high risk people for T2DM

168
Q

Candidates for bariatric surgery (gastric banding or bypass)?

A

BMI >35 + risk factors or BMI >40, failing behaviour modification.

169
Q

Lifestyle modification for obesity?

A
  • Nutrition: reduce energy intake by 500-1000kcal/day
  • Physical Activity: initially 30m of mod intensity 3-5x/wk; eventually >60m on most days – add endurance exercise training
  • Cognitive Behavioural Therapy
170
Q

What are the pharmacologic treatments of obesity?

A
  • Orlistat
  • Contrave (naltrexone and bupropion):
  • Saxenda (liraglutide)
171
Q

What is orlistat and its S/E?

A

GI lipase inhibitor reduces fat absorption by 30% by inhibition of pancreatic lipase. Flatus, oily stools, and diarrhea are common but tend to resolve during the 2nd year of treatment. Avoid with IBD

172
Q

What is contrave (naltrexone and bupropion)?

A

Naltrexone (used to aid in alcohol cessation) is an opioid antagonist and is thought to block negative feedback on satiety pathways in the brain. Bupropion (used to treat depression and aid in smoking cessation) can induce hypophagia by adrenergic and dopaminergic activity in the hypothalamus.

173
Q

What is Saxenda (liraglutide)?

A

GLP-1 (or glucagon-like peptide-1) augments glucose-mediated insulin release from the pancreas to induce glycemic control; liraglutide also stimulates satiety and reduces food intake.

174
Q

Etiology of obesity in pediatrics?

A

Organic causes (rare, <5% - Prader-Willi, Carpenter, Turner, Cushing syndrome, hypothyroidism)

175
Q

Risk Factors of obesity in pediatrics?

A

Genetic predisposition (both parents obese = 80% chance child is)

176
Q

Physical exam findings in obesity in pediatrics?

A

Hypertension, evidence of PCOS, visceral fat deposition, bowing, acanthosis nigricans

177
Q

Investigations for obesity in pediatrics?

A
  • TG, HDL, LDL and cholesterol - Fasting lipid profile in any children older than 2 with obesity
  • Screen for T2D – OGTT or fasting glucose if pre-pubertal with 3 or pubertal with 2 risk factors: high risk ethnic group, another first degree relative with type 2 diabetes, obesity, mom had gestational diabetes, signs of insulin resistance (AN, HTN, dyslipidemia)
  • ALT looking for NAFLD - all children greater than 9 and obese
178
Q

Prevention of obesity in pediatrics?

A
  • <2h/d of sedentary time
  • 1-4y – 180 min/day of physical activity
  • 5-17y – 60 min/day of mod to vigorous physical activity >6 d/wk
179
Q

Treatment of obesity in pediatrics?

A
  • Moderate intensity multidisciplinary programs with parental involvement are effective are reducing BMI and BP
  • Strategies: limit sugar-sweetened beverages, decrease screen time, increase fruit and veggies, increase PA
180
Q

3 main things to look for Cushing’s syndrome?

A
  • Truncal obesity - Increased Deposition of Fat: face, clavicles, back of neck, abdomen. Decreased Deposition of Fat: extremities
  • Violaceous Stretch Marks - Striae
  • Easy Bruising

Others:
 Round face, moon like, increased fat around the face and neck
 Redness of the face – Plethora

181
Q

Causes of Cushing’s syndrome?

A

 Iatrogenic* exogenous steroids* - most common
 ACTH-dependent – pituitary tumor (Cushing’s Disease), ectopic ACTH syndrome, ectopic CRH syndrome
 ACTH-independent (high cortisol, low ACTH) – adrenal adenoma, adrenal carcinoma

182
Q

Confirmatory tests of Cushing’s syndrome?

A
  • Low Dose Dexamethasone Suppression: Measure 24 hr urinary free cortisol levels
  • Lack of Suppression = Cushing’s Syndrome
183
Q

If Cushing’s syndrome is confirmed, what should be measured?

184
Q

Screening tests for Cushing’s syndrome?

A
  • Two 24 hr urine cortisol:creatinine ratio (>30)
  • Overnight 1mg Dexamethasone Suppression Test – take at 11pm - this should result in a low cortisol level less than 50nmo/L in patients without Cushing’s
  • Midnight salivary cortisol - This should naturally be low at midnight in people without Cushing’s
  • With a positive test result, need to confirm test to rule out false positives
185
Q

If ACTH is suppressed (ACTH – independent) when investigating the cause of Cushing’s syndrome, what should you suspect and order?

A

Look at the Adrenals for masses. CT/MRI Adrenals

186
Q

If ACTH is increased (ACTH – dependent) when investigating the cause of Cushing’s syndrome, what should you suspect and order?

A
  • High Dose Dexamethasone suppression test (Pituitary tumours will respond to high dose dexamethasone, slight decrease in cortisol. Ectopic tumor there will be no change to cortisol or ACTH)
  • CRH Test (Pituitary Tumours will respond to CRH)
  • MRI pituitary
  • Bilateral Inferior Petrosal Sinus Sampling - Useful when the MRI pituitary is normal. ACTH should be high around the pituitary (>2x difference between central + peripheral ACTH) if that’s where the source is. But if the levels between the central and peripheral ACTH are the same, then there might be an ectopic tumors outside the pituitary
187
Q

Serum cortisol may appear elevated in patients on the _______ as estrogen increases the cortisol binding protein, and therefore the total measured serum cortisol level.

A

Oral contraceptive pill.

The 24hr urine for free cortisol will be normal in this group as this is measuring free and unbound cortisol.

188
Q

What are the two categories of hypertension?

A

Primary HTN (95%) or secondary HTN (5%)

189
Q

What is primary hypertension?

A

Primary hypertension has no single known cause but several mechanisms are linked to altered pathways in BP control.

190
Q

What is secondary hypertension?

A

In secondary hypertension BP is raised due to a known underlying cause

191
Q

Risk factors for primary hypertension?

A

Age > 30, obesity, FHx (2x), excessive salt intake or fatty diet, African American ancestry, alcohol consumption, sedentary lifestyle, renal failure

192
Q

What is the definition of HTN (including in DM and age >80yr old?

A

HTN - BP ≥140/90 mmHg, unless DM (≥130/80 mmHg), or age ≥80 yr (≥150/90 mmHg)

193
Q

What is the definition of isolated systolic HTN?

A

Isolated systolic HTN - sBP ≥140 and dBP <90, usually begins in 5th decade

194
Q

What is the definition of white coat hypertension?

A

White coat hypertension - high clinic BP with normal home BP and 24 ambulatory BP, caused by anxiety in clinic

195
Q

What is the definition of masked hypertension?

A

Masked hypertension - normal clinic BP with high BP in home and/or ambulatory setting, often provoked by anxiety, job stress, exercise

196
Q

What is the definition of hypertensive urgency?

A

Hypertensive urgency - sBP >180 or dBP >120 with minimal or no target-organ damage

197
Q

What is the definition of severe HTN?

A

Severe HTN (dBP > 120) + acute target-organ damage

198
Q

What are the target end organs for severe HTN?

A

o CNS – cerebral infarct, hypertensive encephalopathy, ICH
o CVS – pulmonary edema, CHF, aortic dissection, acute MI
o Renal
o Retinal involvement
o Eclampsia

199
Q

What is the definition of accelerated HTN ?

A

Accelerated HTN - significant recent increase in BP over previous hypertensive levels associated with evidence of vascular damage on fundoscopy, but without papilledema

200
Q

What is the definition of malignant HTN ?

A

Malignant HTN - sufficient elevation in BP to cause papilledema and other manifestations of vascular damage (retinal hemorrhages, bulging discs, mental status changes, increasing creatinine)

201
Q

When should you suspect a secondary cause of HTN?

A

Suspect if new onset age <30 or >80, if refractory to multiple meds, FHx/PHx kidney disease

202
Q

What are the etiologies of secondary HTN?

A
  • Renovascular: renal parenchymal disease, glomerulonephritis, pyelonephritis, ESRD
  • Endocrine: primary aldosteronism, pheochromocytoma, Cushing’s syndrome, hyper(para)thyroidism, hypercalcemia (any cause)
  • Vascular: coartaction of the aorta (young children), renal artery stenosis
  • Drugs: common (estrogen/OCPs, NSAIDs, steroids, decongestants, EtOH), psych (MAOIs, lithium, amphetamines), illicit drugs (cocaine/other amphetamines)
  • Food: salt, EtOH, licorice root, cocaine
  • Obstructive Sleep Apnea
203
Q

When should you suspect an endocrine cause of secondary HTN?

A

Suspect when: sudden onset/worsening HTN, refractory HTN to 3 or more drugs, abdo bruit, ACEi or ARB ^Creatinine (Cr) by >30%, recurrent pulmonary edema associated with BP spikes, atherosclerotic disease (esp if smoker or dyslipidemia present)

204
Q

When should you suspect a renovascular cause of secondary HTN?

A

Suspect when: refractory HTN to 3 or more drugs, HYPOkalemia (b/c aldosterone resorbs water via Na/K swap) – spontaneous/profound diuretic induced hypokalemia (< 3), adrenal adenomas present

205
Q

What investigations should you do for all patients with HTN?

A

 Renal (lytes, Cr, urinalysis), cardiac (lipid profile, 12-lead ECG), endocrine (fasting glucose, HbA1C), home BPs
 Known Diabetes or CKD: + urinary protein excretion (Albumin:Creatinine Ratio)

206
Q

What investigations should you do if you suspect hypercalcemia as the cause of secondary HTN?

A

Suspect Hypercalcemia: Ca and albumin

207
Q

What investigations should you do if you suspect renovascular HTN?

A

Suspect Renovascular HTN (abdominal bruit): + renal U/S + captopril renal scan (if GFR>60) +/- MRA/CTA (if good renal function)

208
Q

What investigations should you do if you suspect aortic coarctation as the cause of secondary HTN?

A

Suspect Aortic Coarctation: ABI and CXR

209
Q

What investigations should you do if you suspect pheochromocytoma as the cause of secondary HTN?

A

Suspect Pheochromocytoma: 24h urine metanephrines, hematocrit (hemoconcentration)

210
Q

What investigations should you do if you suspect OSA as the cause of secondary HTN?

A

Suspect OSA: Sleep study with O2 saturations

211
Q

What investigations should you do if you suspect cardiac as the cause of secondary HTN?

A

Suspect Cardiac Cause/Complications: + echocardiogram (look for LV function)

212
Q

What investigations should you do if you suspect Cushings as the cause of secondary HTN?

A

Suspect Cushings: 24hr cortisol + low dose DEXA scan

213
Q

What investigations should you do if you suspect primary hyperaldosterone as the cause of secondary HTN?

A

Suspect Primary Hyperaldosterone: serum aldosterone/renin ratio

214
Q

What should you do for physical exam for HTN?

A
  • General Appearance: look for Cushingoid appearance (striae, acne, hirsutism, obesity, buffalo hump), and look for pheochromocytoma appearance (sweaty, anxious, flushed)
  • Head & Neck: fundoscopy (arteriolar narrowing, hemorrhages, exudates, papilledema)
  • Neck: hyperthyroidism (goitre), carotid bruits, JVP
  • CVS: LVH (displaced, diffuse, sustained apex beat), hyperthyroid/pheochromocytoma (^HR), evidence of CHF (crackles, S3) or LVH (S4), aortic dissection (check BP in both arms for pulse deficit, and neuro signs)
  • Abdomen: look for Cushingoid appearance (striae), renovascular HTN (renal bruits), PVD (femoral bruits), PKD (renal masses, or abnormal aortic pulsations)
  • Extremities: peripheral edema, peripheral pulses
  • Neuro: examine for signs of a stroke
215
Q

What should you ask on history for HTN?

A

o The duration of hypertension, previous attempts at treatment
o Complications (ischemic heart disease, peripheral arterial disease, left ventricular hypertrophy, stroke, TIA, microalbuminuria or proteinuria, and chronic kidney disease)
o Cardiac risk factors (smoking, diabetes, dyslipidemia, obesity)
o Past medical history (thyroid, renal, or adrenal disorders)
o Medications (antihypertensives, steroids, illicit drugs)

216
Q

If automated office BP (AOBP) < 135/85 on 1st visit?

A

No HTN, annual BP measurement recommended

If higher than these cut offs, then out-of-office assessment needed, ABPM* or HBPM

217
Q

What BP can you diagnosis HTN on the 1st visit?

A

If BP >180/110 = HTN

218
Q

If office blood pressure measure (OBPM) < 140/90 on 1st visit?

A

No HTN, annual BP measurement recommended

If higher than these cut offs, then out-of-office assessment needed, ABPM* or HBPM

219
Q

If on visit 2 (w/n 1 month), Daytime ABPM or HBPM <135/85?

A

Whitecoat HTN, repeat/annual BP measurement recommended

If higher than these cut offs, then HTN

220
Q

If on visit 2 (w/n 1 month), if 24h ABPM <130/80?

A

Whitecoat HTN, repeat/annual BP measurement recommended

If higher than these cut offs, then HTN

221
Q

What are some lifestyle management options for HTN?

A

Lifestyle: diet (DASH – low cholesterol, low saturated fats + Canada Food Guide, lower Na+ intake to 2000mg, no Mg/Ca supplements), exercise (30-60min moderate intensity 4-7x/wk), social (no smoking, less EtOH <2 drinks a day, less stress via CBT), weight loss (maintain BMI 18-25 and waist <102cm for men and <88cm for women)

222
Q

First line medication for patients with diabetes and elderly with HTN?

223
Q

S/E of ACEi (ramipril)?

A

Side Effects: cough, angioedema, hyperkalemia, hypotension, dizziness

224
Q

Contraindications of ACEi?

A

Contraindications: bilateral renal artery stenosis + pregnancy + reduced GFR/pre-renal AKI; when BP drops, usually afferent renal artery drops tone (dilates), so more systemic pressure goes into the glomerulus. ACEi blocks this, so then the afferent artery constricts and the kidneys can’t perfuse as well, leading to an AKI…pre-renal AKI + ACE = poor renal perfusion

225
Q

S/E of ARBs (valsartan)?

A

Side Effects: cough, angioedema, hyperkalemia, hypotension, dizziness

226
Q

Contraindications of ARBs?

A

Contraindications: bilateral renal artery stenosis + pregnancy + history of angioedema

227
Q

S/E of Calcium Channel Blockers (amlodipine)?

A

Side Effects: flushing, constipation, bradycardia, hypotension, palpitations

228
Q

S/E of diuretics (thiazide)?

A

Side Effects: dehydration, hyponatremia/hypokalemia/hypomagnesemia, hypercalcemia, hypertriglyceremia

229
Q

HTN medication: Only if age <60, not first line if older

A

Beta-Blockers

230
Q

S/E of Beta-Blockers?

A

Side Effects: fatigue, bradycardia, syncope, angina

231
Q

If first line monotherapy only has partial effect for HTN then what?

A

ADD ANOTHER FIRST LINE (DIFFERENT CLASS, B Last)

232
Q

Don’t use thiazide diuretics in _______, esp. as monotherapy.

A

hypokalemia

They block Na/Cl symport at the distal collecting duct, so the aldosterone sensitive Na/K antiporter in the duct goes into overdrive and dumps all the K+ into the urine; similar to why furosemide (Lasix) cause hypokalemia

233
Q

What should be your follow up with an individual diagnosed with HTN?

A

Medication Follow-Up: q1-2 months until BP at target for 2 consecutive visits; q3-6 months after

234
Q

What is the Ddx for malignant HTN?

A

o Malignant HTN
o Hypertensive encephalopathy (most common)
o CVA - ischemia or hemorrhagic
o SAH, aortic dissection, MI/ischemia, acute pulmonary edema, renal failure, acute refractory LV failure

235
Q

What should your target be in dropping BP in HTN emergencies?

A

Aim to drop 25% over hours. <180/<120 for the first hour, and <160/<110 for the next 23 hours

Do not aggressively treat; brain gets accustomed to high BP, too fast = hypotensive stroke

236
Q

What are the medications used for HTN emergencies?

A

Labetalol (most common), nitroprusside, hydralazine.

237
Q

What investigations should you do for hyponatremia?

A

Serum electrolytes, glucose, Cr, BUN, osmolality, Urine sodium, osmolality, Volume status

238
Q

What is a complication you must consider when correcting acute situations of hyponatremia?

A

Cerebral edema

239
Q

What is the treatment of hypernatremia?

A
  • Replace H20 (Fluids – Encourage patient to drink pure water, as oral route is preferred for fluid administration
  • If unable to replace PO or NG, correct H2O deficit with hypotonic IV solution (IV D5W, 0.45% NS [half normal saline], or 3.3% dextrose with 0.3% NaCl [“2/3 and 1/3”])
  • Consider adding ADH. Oral is better then parenteral.
240
Q

Treatment of chronic hypernatremia?

A

Aim to lower serum sodium by - 10mEq/L in 24h (often achieved by giving free water at 1.35 mL/kg/h)

241
Q

Treatment of acute hypernatremia?

A

Use formula to calculate water deficit. Replace entire water deficit within 24 hr (hourly infusion rate = water deficit in mL/24 h)

242
Q

H20 Deficit Equation

A

TBW = 0.6 x wt (kg) men TBW = 0.5 x wt (kg) women

H2O deficit = TBW x ([Na+]plasma – 140) / 140

243
Q

What is the treatment of SIADH?

A
  • Severe water restriction (eg, 250 to 500 mL/24 hours) is generally required.
  • A loop diuretic may be combined with IV 0.9% saline as in hypervolemic hyponatremia (no more than 4 to 6 mmol/L which should be done over 4 to 6 hours)
  • Treat cause or stop offending meds
  • If underlying disorder is not correctable - demeclocycline inducing a concentrating defect in the kidneys
  • Vaptans - a selective vasopressin receptor antagonist
244
Q

What is the treatment of hypervolemic hyponatremia?

A

Fluid restrict, sometimes a diuretic, occasionally a vasopressin antagonist

245
Q

What is the treatment of hypovolemic hyponatremia?

A

Normal saline (<8 mmol/L) over the first 24 hours

246
Q

What are the 3 categories of hyponatremia?

A

Iso-osmolar hyponatremia
Hypo-osmolar hyponatremia
Hyperosmolar hyponatremia

247
Q

What are the symptoms of hypernatremia?

A 
Dehydration – thirst
CNS dysfunction (brain cell shrinkage) – altered mental status, confusion, neuromuscular excitability, seizures, or coma
248
Q

What would cause hypo-osmolar hyponatremia?

A

Hypervolemic:

  • Urine Na <20mEq/L - CHF, cirrhosis or nephrotic syndrome *Lower circulating volume increasing the release of aldosterone and ADH
  • Urine Na >20mEq/L – Renal (ARF, CRF)

Euvolemic:

  • Dilute urine – adrenal insufficiency or drinking too much water (1. psychogenic polydipsia (excess H20 consumption) 2. beer potomania or “tea + toaster” (disproportionate nutritional intake in form of fluid))
  • Concentrated urine (high urine osmolarity) – SIADH (increased urine [Na+], Dx of exclusion)

Hypovolemic:

  • Extrarenal loses (GI, skin, lung) – urine Na < 10 mmol/L
  • Renal losses (diuretics, salt-wasting nephropathy)
249
Q

What helps determine the cause of hypernatremia?

A

Urine osmolality

250
Q

How does glucose effect the serum concentration of Na?

A

Every 10mmol/L increase serum glucose above 10, drop in serum [Na+] by 3mmol/L.

251
Q

What causes hyperosmolar hyponatremia?

A

Hyperglycemia or mannitol

252
Q

Which hypo-osmolar hyponatremia would cause edema + ascites?

A

Hypervolemic

253
Q

If urine osmo >500 then what would be considered the cause?

A

Non-renal causes or water loss (GI, respiratory, skin losses, insensible)

254
Q

What would cause iso-osmolar hyponatremia?

A

Pseudohyponatremia – due to hyperlipidemia/proteinuria

255
Q

What are the symptoms of hyponatremia?

A

Neurologic symptoms predominate (secondary to cerebral edema): headache, nausea, malaise, lethargy, weakness, muscle cramps, anorexia, somnolence, disorientation, personality changes, depressed reflexes, decreased LOC
In chronic cases - asymptomatic

256
Q

If urine osmo 250-500 and <250 then what would be considered the causes?

A

o 250-500 – diuretics

o <250 - DI

257
Q

What are the causes of hypernatremia?

A

Hypovolemic:
• GI loss (diarrhea)
• Reduced intake (elderly, coma, surgical)
• Diuretic (high urine osmo)
• Hyperglycemia
Euvolemic:
• Insensible losses (sweating)
• Diabetes Inspidus (lack ADH) (low urine osmo). Could be central or nephrogenic (ADH issue).
Hypervolemic:
• Excessive administration of hypertonic sodium bicarbonate

258
Q

In chronic hyponatremia (>24h), we can anticipate brain cells have adapted by losing osmoles and so if we add them back too quick, brain cells might shrink too much inducing

A

Osmotic demyelination syndrome

259
Q

Definition of hypercalcemia?

A

Definition: total corrected serum Ca2+ >2.6 mmol/L OR ionized Ca2+ >1.35 mmol/L

260
Q

Symptoms and signs of hypercalcemia?

A

 Psychiatric – psychosis (MOANS)
 Neurologic: hypotonia, hyporeflexia, myopathy, paresis
 Gut effects – constipation, nausea, vomiting (GROANS), anorexia, abdominal pain
 Renal effects – polyuria (osmotic diuresis), chronic – renal stones (STONES)
 MSK – bone pain (BONES), weakness
 CV – arrhythmias, asystole
 → “moans, bones, groans, and psychic overtones”

261
Q

Causes of hypercalcemia?

A

Calcium excess, hyperparathyroidism, immobility, iatrogenic (thiazide diuretics), milk-alkali syndrome (usually during self-treatment with calcium carbonate antacids for dyspepsia), Paget’s disease, Addison’s disease, neoplasms (lung) and metastases (breast or prostate) and MM, Zollinger Ellison Syndrome, Excess vit D, Excess vit A, sarcoidosis

262
Q

Most common cause of hypercalcemia in outpatient?

A

Hyperparathyroidism 1 – most common in outpatient

263
Q

Most common cause of hypercalcemia in inpatient?

A

Malignancy

264
Q

How to differentiate between primary hyperparathyroidism and familial hyperparathyroid syndromes?

A

Urinary calcium excretion (24-hour urinary calcium or calcium-to-creatinine ratio) should be measured to differentiate between familial hypocalciuric hypercalcemia

265
Q

In your approach to the etiology of hypercalcemia what should you measure first?

A

PTH for PTH mediated hypercalcemia:
o Elevated - Primary hyperparathyroidism - Excess PTH from autonomous benign adenomas
o Mid- upper normal - Primary hyperparathyroidism likely or familial hyperparathyroid syndromes.
o Low-normal low (non-PTH mediated hypercalcemia)

266
Q

In the presence of low serum PTH concentrations, what should be measured to assess for hypercalcemia?

A

In the presence of low serum PTH concentrations (<20 pg/mL), PTH-related protein (PTHrp) and vitamin D metabolites should be measured to assess for hypercalcemia of malignancy and vitamin D intoxication

267
Q

An elevated serum concentration of 25(OH)D is indicative of?

A

Vitamin D intoxication due to the ingestion of either vitamin D or calcidiol itself

268
Q

Definition of dyslipidemia?

A

Elevated cholesterol +/or triglycerides, or low HDL, associated with atherosclerosis

269
Q

Etiology of dyslipidemia?

A

o Primary: Genetic - Familial hypercholesterolemia, ApoC2 Deficiency
o Secondary

270
Q

Secondary causes of Hypertriglyceridemia?

A
  • Endocrine: Obesity/metabolic syndrome Diabetes
  • Lifestyle: Alcohol, high carbohydrate/ high fat diet
  • Drugs: corticosteroids, estrogen, hydrochlorothiazide, retinoic acid, β-blockers without intrinsic sympathomimetic action (ISA), anti- retroviral drugs, atypical antipsychotics, oral contraceptive pills
  • Other: pregnancy
271
Q

Secondary causes of Low LDL?

A
  • Endocrine: obesity/metabolic syndrome, DM
  • Drugs: β-blockers, anabolic steroids
  • Other: acute infections, inflammatory conditions
272
Q

Secondary causes of Hypercholesterolemia?

A
  • Endocrine: hypothyroidism
  • Renal: nephrotic syndrome, chronic kidney injury
  • Immunologic: monoclonal gammopathy
  • Hepatic: cholestatic liver disease (PBC)
  • Nutritional: Anorexia nervosa
  • Drugs: cyclosporin, carbamazepine
273
Q

Increased HDL is associated with ____ cardiovascular disease and mortality

274
Q

Symptoms and signs of dyslipidemia?

A

o Dyslipidemia itself usually causes no symptoms but can lead to symptomatic vascular disease, including coronary artery disease (CAD), stroke, and peripheral arterial disease.
o High levels of triglycerides (> 500 mg/dL [> 5.65 mmol/L]) can cause acute pancreatitis. Very high triglyceride levels can also cause hepatosplenomegaly, paresthesias, dyspnea, and confusion.

275
Q

Investigations of dyslipidemia?

A

o Only individuals with hypertriglyceridemia (TG >4.5 mmol/L) require a fasting lipid panel
o Lipid Panel (measured total cholesterol, TG, and HDL cholesterol and calculated LDL cholesterol and VLDL cholesterol)
o Patients >40 old with no HbA1c in past 3 years: HbA1c
o Others: Creatinine, Fasting glucose, Liver enzymes, Thyroid-stimulating hormone (TSH), Urinary protein

276
Q

Who should receive screening for dyslipidemia?

A
  • nLipid testing is part of global CVD risk estimation in men >40 years and women >50 years of age and is repeated every 5 years. Non-fasting lipid levels can be obtained
  • Consider screening at earlier age for patients who have known traditional cardiovascular risk factor(s) including, but not limited to, hypertension, family history of premature CVD, diabetes, and smoking.
277
Q

Estimates 10-year risk of heart attack

A

Framingham risk calculator

278
Q

Framingham risk calculator estimates risk based off?

A

Calculated based on gender, age, total cholesterol, HDL, sBP, and smoking

279
Q

What are statin-indicated conditions?

A 
o	If you have an LDL-C > 5.0mmol/L  or documented familial hypercholesterolemia
o	Clinical atherosclerosis (MI, ACS, stable angina, stroke/TIA, PAD, claudication and/or ABI <0.9, documented carotid disease)
o	Abdominal Aortic Aneurysm
o	DM (>40 years old, or >15 years duration and age >30 years or microvascular complications)
o	Chronic kidney disease (> 3months duration and ACR >3.0 mg/mmol or eGFR <60)
280
Q

Start treatment for dyslipidemia if:

A

• High risk patient (FRS >20%) = Use high potency statin + consider ASA
• Intermediate risk patients (FRS 10-19%) AND = Use moderate potency statin
● LDL >3.5 mmol/L OR
● Non-HDL-C >4.3 mmol/L OR
● Apo-B >1.2 g/L OR
● A man >50 years old or a woman >60 years old and they have 1 additional CVD risk factor (low HDL-C, impaired fasting glucose, smoker, HTN)

281
Q

For patients with a 10-year CVD risk of <10%

A

Re-test lipids in five years with risk estimation and encourage lifestyle interventions

282
Q

How much can health behaviours decrease LDL-C by?

A

Health Behaviours: can decrease LDL-C by up to 10%

283
Q

Health behaviours for the treatment of dyslipidemia?

A
  • Smoking Cessation: probably the most important for preventing CAD
  • Dietary Modification: Mediterranean diet: reduce saturated fat, red meat, refined sugar, alcohol; consume nuts, fruits/vegetables, poultry, fish
  • Physical Activity: at least 150 min of moderate to vigorous intensity aerobic exercise per wk
  • Employ consistent lifestyle modifications for at least 3 mo before considering drug therapy; high risk patients should start treatment immediately with concurrent health behaviour interventions
284
Q

1st line therapy for dyslipidemia?

A

1st Line Therapy: statins (HMG-CoA reductase inhibitors)

285
Q

MOA of statins?

A

Inhibit cholesterol synthesis (HMG CoA reductase inhibitors), increase LDL receptor therefore they grab more LDL from the blood

286
Q

Moderate intensity statins?

A

Moderate intensity: Atorvastatin 10-20mg; Rosuvastatin 5-10mg

287
Q

High intensity statins?

A

High intensity: Atorvastatin 40-80mg; Rosuvastatin 20-40mg

288
Q

S/E of statins?

A
  • Potential side effects: myopathy (most common), increased liver enzymes, abdominal pain, rhadomyolysis and elevation of blood glucose levels
  • Increases in creatine kinase (CK) and liver enzymes in asymptomatic patients can occur, and many of these enzyme elevations will return to baseline with continued statin use.
289
Q

Contraindications to statins?

A

Contraindications: severe liver disease + pregnancy

290
Q

Add-On therapies for dyslipidemia?

A
  • Ezetimibe

- PCSK9 inhibitors

291
Q

MOA of ezetimibe

A

Inhibits gut absorption of cholesterol

292
Q

When should ezetimibe be used?

A
  • Used for patients intolerant to statins or statin is contraindicated OR
  • Failure to achieve target LDL with statin at maximum dose
293
Q

Potential side effects of ezetimibe?

A

Potential side effects: myopathy, abdominal pain, rhadomyolysis

294
Q

Who should be offered ASA as primary prevention with dyslipidemia?

A
  • DO NOT prescribe ASA for patients without previous CVD and an estimated 10-year CVD risk <20%.
  • Offer ASA for primary prevention in patients with a 10-year CVD risk >20% and bleeding risk is considered low.
  • Consider ASA for primary CVD prevention after statin therapy has been discussed.
295
Q

Familial hypercholesterolemia pathophysiology?

A

LDL receptor defect. Diminished LDL clearance

296
Q

Clinical features of familial hypercholesterolemia?

A

Tendon xanthomas (achilles, patellar and extensor of hands, arcus corneae, premature CAD (ages 30–50), responsible for about 5% of MIs in people < 60 years

297
Q

Treatment of familial hypercholesterolemia?

A

Diet, Lipid-lowering drugs, LDL apheresis (for homozygotes and heterozygotes with severe disease), Liver transplantation (for homozygotes)

298
Q

What is ApoC2 deficiency

A

ApoC2 deficiency: prevents activation of lipoprotein lipase leading to massive accumulation of triglyceride

299
Q

Clinical features of ApoC2 deficiency?

A

Adolescence to adulthood (APOC2) - Abdominal complaints (pain, hepatosplenomegaly, pancreatitis), Eruptive xanthomata

300
Q

Treatment of ApoC2 deficiency?

A

Diet: Severe fat restriction with fat-soluble vitamin supplementation and medium-chain TG supplementation

301
Q

Definition of isolated hypertriglyceridemia?

A

Mild ≥2.2 mmol/L (≥200 mg/dL) vs. marked ≥5.6 mmol/L (≥500 mg/dL)

302
Q

Does isolated hypertriglyceridemia increased CVD risk?

A

Does not increase cardiovascular risk

303
Q

Treatment of isolated hypertriglyceridemia?

A

Pharmacotherapy: nicotinic acid or fibrates (used to prevent pancreatitis, NOT CVD!)

LMCC (23 decks)

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