FINAL CV/renal

Question 1

What is HTN?

Answer 1

Home BP of135/ 85 or greater

Question 2

Risk factors for HTN

Answer 2

Increasing age, obesity, smoking, family hx, high sodium diet (>3g Na increases BP), excessive ETOH, physical inactivity, glucose intolerance

Question 3

______ in 4 Canadians will have hypertension

Answer 3

1/4 Canadians will have HTN

Question 4

Time course of HTN?

Answer 4

Usually develops gradually over a long period of time (months to years). Usually chronic.

Question 5

Patho of HTN?

Answer 5

Complex. Since BP= COx SVR, anything causing increased blood volume or increased vascular resistance will cause increased BP.

Shift in the pressure natriuresis relationship means there is an increase in vascular volume due to decrease in renal salt excretion. Caused by many factors (genetics, increased SNS response, decreased dietary potassium, magnesium, calcium, increased dietary sodium, insulin resistance, obesity, renal glomerular/ tubular inflammation, dysfunctional natriueretic hormones, increased RAAS response, endothelial dysfunction)

Increased SNS response causes HTN by increased HT and systemic vasoconstriction, increasing renin and angiotensin levels, causing insulin resistance, and inducing vascular remodelling.

Question 6

S&S HTN

Answer 6

usually no overt symptoms. Sometimes may include dizziness, headaches, visual problems, shortness of breath

Question 7

Dx of HTN

Answer 7

Mean AOBP BP > 180/ 110 (automated office blood pressure)
ABPM daytime mean >135/ 85 or 24 hour mean >130/80 (Ambulatory blood pressure monitoring)
HBPM series mean >135/85 (Home blood pressure monitoring)

Question 8

Preferred BP method to diagnose HTN?

Answer 8

ABPM (ambulatory blood pressure monitoring) (out of office)

Question 9

Can HTN be diagnosed solely based on AOBP (automated office blood pressure)

Answer 9

Yes if >180/ 110
Otherwise no, need out of office measurement to rule out white coat HTN
(ABPM >135/85 daytime mean or >130/80 24 hour mean OR HBPM > 135/85)

Question 10

George has diabetes and comes in with a blood pressure of 160/ 79. What should the provider do next to diagnose HTN?

Answer 10

Check OBPM (office blood pressure measure- electronic upper arm device with provider in room) on 3 different days. If these measurements are >130/80, he probably has HTN. However, he needs out of office BP measurement to rule out white coat HTN. If his ABPM is >135/85 (daytime mean) or >130/8- (24 hour mean) OR his HBPM is >135/ 85 then he will be diagnosed with HTN.

Question 11

Sally does not have diabetes, but comes in with a blood pressure of 155/ 89. What should you do to diagnose HTN?

Answer 11

If AOBP (automated BP measured with provider not in room) is >135/85) or OBPM (automated BP measured with provider in room) is >140/90, the pt likely had HTN but need out of office measurement to rule out WCH. Sally will be diagnosed with HTN if her ABPM is >135/85 (daytime mean) or >130/80 (24 hour mean) or HBPM is >135/ 85

Question 12

Besides measuring BP, what else should be checked in diagnosing HTN?

Answer 12

Routine labs, including urinalysis for proteinemia, blood chemistry cholesterol, triglycerides, ECG, history taking (risk factors like fam hx, etoh, smoking, dietary and physical activity, etc.)

Question 13

What end organ damage can occur due to HTN?

Answer 13

Cardiovascular disease (CAD, ACS, angina, HF, LV dysfunction, LV hypertrophy)
Cerebrovascular disease (aneurysmal SAH, carotid artery disease, intracerebral hemorrage, ischemic stroke or TIA, dementia)
Hypertensive retinopathy
Peripheral artery disease (intermittent claudication, lower extremity trophic changes)
Renal disease (CKD, albuminuria)

Question 14

How can HTN lead to stroke?

Answer 14

Reduced blood flow and oxygen supply, weakened vessel walls, accelerated atherosclerosis. Causes TIAs, cerebral thrombosis, aneurysm, hemorrage, and acute brain infarction

Question 15

How can HTN lead to retinopathy?

Answer 15

Retinal vascular sclerosis and increased retinal artery pressures lead to hypertensive retinopathy, retinal exudates, and hemorrages

Question 16

How can HTN lead to aneurysm?

Answer 16

Weakened vessels walls and higher artery pressures

Question 17

How can HTN lead to renal disease?

Answer 17

Reduced blood flow, increased arteriolar pressure, RAAS and SNS stimulation, inflammation lead to glomerulosclerosis, decreased glomerular filtration, ESRD.

Question 18

How can HTN lead to heart failure?

Answer 18

Increased afterload increases the workload of the heart combined with diminished blood flow through coronary arteries. As a response, LV hypertrophy occurs, myocardial ischemia results, and HF may develop.

Question 19

Phases of hypertensive retinopathy?

Answer 19

Vasoconstrictive- microvascular retinal changes occur in response to acute/ chronic HTN
Sclerotic- structural changes consistent with arteriosclerosis. Endothelial wall damage is seen.
Exudative- Blood retina barrier is disrupted and can lead to smooth muscle necrosis. Leaking blood and plasma can obliterate the vascular lumen.

Poor perfusion can lead to atrophy, ischemia, and even retinal detachments.

Question 20

Repeat the phases of hypertensive retinopathy

Answer 20

Vasoconstrictive
Sclerotic
Exudative

Question 21

________ is the most common cause of chronic kidney disease and end-stage kidney disease.

Answer 21

Diabetes

Approximately 50% of individuals with diabetes mellitus develop diabetic kidney disease

Question 22

ESRD is considered a GFR of <

Answer 22

<15ml/min

Question 23

What are some signs and symptoms of severe kidney damage (GFT 15-29ml/min)

Answer 23

Erythropoietin deficiency anemia Hyperphosphatemia
Increased triglycerides Metabolic acidosis Hyperkalemia
Salt or water retention

(plus HTN, inc creatinine and urea…which are some of the earlier signs that appear)

Question 24

Skeletal effects of chronic kidney disease

Answer 24

Spontaneous fractures and bone pain
Deformities of long bones

Mechanism of this:
Osteitis fibrosa –> bone inflammation with fibrous degeneration related to
hyperparathyroidism
Osteomalacia –> bone resorption
associated with vitamin D and calcium
deficiency

Question 25

Cardiopulmonary effects of CKD inlclude Pulmonary edema and kussmaul respirations. Why do these occur?

Answer 25

Fluid overload associated with pulmonary
edema and metabolic acidosis leading to
Kussmaul respirations

Question 26

What does Kussmaul breathing look like?

Answer 26

Kussmaul breathing is a deep and labored breathing pattern often associated with severe metabolic acidosis, particularly diabetic ketoacidosis (DKA) but also kidney failure. It is a form of hyperventilation, which is any breathing pattern that reduces carbon dioxide in the blood due to increased rate or depth of respiration.

Question 27

How does CKD lead to heart disease?

(this includes left ventricular hypertrophy, cardiomyopathy, and ischemic
heart disease; hypertension, dysrhythmias, accelerated atherosclerosis; pericarditis with fever, chest pain, and pericardial friction rub)

Answer 27

Extracellular volume expansion and
hypersecretion of renin associated with
hypertension

anemia increases cardiac workload;

dyslipidemia promotes
atherosclerosis;

toxins precipitate into
pericardium

Question 28

WHy does encephalopathy result from CKD?

Answer 28

Progressive accumulation of uremic
toxins associated with end-stage
kidney disease (ESKD)

Question 29

How does CKD lead to anemia?

Answer 29

Reduced erythropoietin secretion and
reduced red cell production; uremic toxins
shorten red blood cell survival and alter
platelet function

Question 30

In CKD, retention of metabolic acids and other waste products leads to GI symptoms. What do these include?

Answer 30

Anorexia, nausea, vomiting; mouth ulcers, stomatitis, urine
odour of breath (uremic fetor), hiccups, peptic ulcers, gastrointestinal bleeding, and pancreatitis associated with ESKD

Question 31

What skin changes occur in CKD?

Answer 31

Abnormal pigmentation (sallow) and pruritis, uremic “frost” (with super high levels of urea that are deposited through sweat)

Retention of urochromes, contributing to
sallow yellow colour; high plasma calcium
levels and neuropathy associated with
pruritus

Question 32

What two conditions are the most common cause of nephron loss

Answer 32

HTN and DM

Question 33

Outline the 5 stages of chronic kidney disease

Answer 33

Stage I: Normal Kidney Function\ Normal or high GFR (>90ml/min)

Stage II: Mild Kidney damage/mild reduction in GFR <60-89ml/min)

Stage III: Moderate Kidney damage/ (GFR 30-59ml/min)

Stage IV: Severe kidney damage/ (GFR 15-29 ml/min)

Stage V: End-Stage kidney disease/ (GFR < 15ml/min)

Question 34

Outline the early stages of CKD. Is it symptomatic? Why might you see an INCREASE in the GFR?

Answer 34

GFR may increases in functional nephrons (due to glomerular hyperfiltration)

Clinical signs minimal/absent

May see HTN

May see increase in Creatine and BUN levels

Question 35

Sorry but here’s a massive list of end-stage symptoms for CKD: (most is repeat from previous questions except contains list of lyte and hormonal changes at the bottom)

Answer 35

Skeletal:
Spontaneous fractures/bone pain

Cardiopulmonary:
Dyspnea, Pulmonary Edema

Cardiovascular:
HTN (80 % of patients), Chest pain, Cardiomyopathy

Neurological:
Encephalopathy or neuropathic pain

Hematological:
Anemia (normocytic), due to reduction of erythropoietin production

Gastro – Intestinal:
Nausea, vomiting, urine odour of breath, mouth ulcers

Integumentary:
Abnormal pigmentation and pruritus
Uremic “Frost”

Endocrine and Reproductive:
Sexual disfunctions
Alteration thyroid hormone metabolism (uremia causing a delay in response of stimulating thyroid hormone receptors)

Electrolyte and Acid Imbalances:
Hyperkalemia (causing muscle weakness, ECG changes)
Hypocalcemia
Hyperphosphatemia
Metabolic acidosis (causing bone deformation/loss)

Question 36

Is the damage done to kidney nephrons in CKD reversible?

Answer 36

No, it is irreversible

Question 37

Patho of CKD (talks about why we see glomerular hyperfiltration, proteinuria)

Answer 37

Loss of nephrons: causes blood flow to shift to functional nephrons creating glomerular hyperfiltration (=kidney is trying to compensate for nephron loss)
- Hyperfiltration will over time lead to further glomerular sclerosis and result in more loss of nephrons
- Repeated injury to the kidney impacts epithelial cell’s ability to reproduce contributing to glomerular sclerosis and tubuinterstitial fibrosis

Factors advancing renal disease:
- Hyperfiltration also leads to proteinuria which activates the inflammatory process and fibrosis leading to tubulointerstitial injury
- Angiotensin II (activated by RASS system) cause glomerular HTN and hyperfiltration. Increased pressure within the glomerulus increases glomerular capillary permeability which also promotes proteinuria

Question 38

What is urine ACR and why is it useful for diagnosing CKD?

Answer 38

Albumin-to-creatinine ratio (ACR) is the first method of preference to detect elevated protein. The recommended method to evaluate albuminuria is to measure urinary ACR in a spot urine sample. ACR is calculated by dividing albumin concentration in milligrams by creatinine concentration in grams.

(sometimes done as 24 hour collection)

Question 39

What 2 lab results inform a diagnosis of CKD (with their values)?

Answer 39

ACR Elevated (>3.0 mg/mmol)
Estimated GFR (eGFR): < 60 mL/min (over at least three months)

eGFR Values of > 60 mL/min per 1.73m2 without other indications for kidney disease (albuminuria, hematuria, structural abnormalities are not indicative for CKD

Question 40

Other important lab values/imaging we would consider for diagnosis of CKD?

Answer 40

Urinalysis:
Continued presence of WBC or RBC
Presence of casts (waxy)
Presence of Protein and Glucose

Other tests to consider:
Electrolytes: K+ increased,
Ca decrease. Na+ increased
Creatine: increased
Blood Urea Nitrogen (BUN): increased
Phosphate levels: increased

Imaging:
Ultrasound: to look at size and structural abnormalities (small fibrotic kidney size)