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Pathology Term 4 > Week 4 - CHF > Flashcards

Week 4 - CHF Flashcards

HTN, Cor Pulmonale

1
Q

What % of the population is affected by HTN and what % are aware of it?

A
  • affects 25% of population
  • less than 35% aware (commonly asymptomatic)
  • occipital headache is the commonest clinical sign
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2
Q

What are the common clinical signs (if present) of HTN?

A
  • dizziness
  • headache (occipital)
  • visual difficulties

*late stage

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3
Q

What is the leading risk factor for MI, stroke and AS?

A

HTN

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4
Q

What can HTN ultimately lead to and how?

A

Chronic organ damage (heart, kidney, brain, eye)

  • *BV damage**
  • macroangiopathy (atherosclerosis - large/med art.)
  • microangiopathy (artereolosclerosis - arterioles + cap)
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5
Q

Outline the physiology of normal BP control

A

BP = CO x TPR

CO:
-blood volume (Na, mineralocorticoids, ANP) + cardiac factors (HR, contractility

TPR:

  • humoral factors
  • neural factors
  • local factors
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6
Q

What are the humoral factors affecting TPR?

A

Constrictors:

  • AT II
  • catecholamines
  • thromboxane
  • leukotrienes
  • endothelin

Dilators:

  • prostaglandins
  • kinins
  • NO
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7
Q

What are the neural factors affecting TPR?

A

Constrictors:
-alpha-adrenergic

Dilators:
-beta-adrenergic

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8
Q

What are the local factors affecting TPR?

A

-autoregulation, pH, hypoxia

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9
Q

What is diagnostic BP for hypertensive emergency?

A 
>/= 180 - systolic
>/= 110 - diastolic
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10
Q

What is diagnostic BP for hypotension?

A

<90 / <60

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11
Q

What are the 2 types of HTN and what is the commonest?

A
  1. L/systemic HTN:
    - essential (primary)** commonest –> 95% (AKA idiopathic –> increased peripheral resistance
    - secondary (renal, CVS, neuro + endocrine causes) –> 5%
  2. R/pulmonary HTN:
    - chronic –> cor pulmonale (lung disease i.e. COPD)
    - acute –> pulmonary embolism
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12
Q

What does L + R sided HTN cause?

A

systemic HTN = LVH
pulmonary HTN = RVH

**guideline = >2cm dilatation in thickness of ventricular wall (normally 1.3cm)

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13
Q

What is the normal gm of LV and what is it after systemic HTN causes LVH?

A 
normal = 350gm
LVH = 500gm
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14
Q

True or False?

-LA dilatation can occur in L-sided HTN

A

True

  • late stage
  • can cause fibrillation
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15
Q

What is the prognosis for L-sided HTN/LVH?

A
  • asymptomatic (compensated)
  • progressive IHD
  • renal damage, stroke
  • progressive CHF/SCD
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16
Q

What is the prognosis for pulmonary HTN/RVH?

A
  • asymptomatic (compensated)

- hepatic congestion (nutmeg) –> Cor pulmonale

17
Q

What are the 2 types of microangiopathy?

A
  1. hyaline arteriolosclerosis –> protein deposition (DM)

2. hyperplastic arteriolosclerosis –> SMC proliferation (HTN)

18
Q

What are the 4 grades of hypertensive retinopathy?

A
  1. thickening of arterioles
  2. focal arteriolar spasms (AV nipping)
  3. haemorrhages (flame), hard waxy exudates (lipid disposit), cotton wool spots (ischaemia/soft exudates)
  4. papilloedema (oedema of optic disc
19
Q

What is the result of chronic HTN on gross kidney appearance?

A
  • “grain/leather kidney”
  • small/shrunken kidney
  • scarred/pitted due to microangipathy + micro-infarcts (glomerular scarring) in cortex of kidney
20
Q

What does malignant HTN cause in the kidneys?

A
  • rapid rise in BP
  • causes acute necrosis and rupture of arterioles (necrotizing arteriolitis) causing pinpoint haemorrhages (c.f. arteriolosclerosis) –> “flea-bitten kidney”
  • renal failure w high mortality
21
Q

What BP is seen in malignant HTN?

A

> 200/120mmHg

22
Q

Where is the commonest site of BV rupture and why?

A
  • cerebral vessles (brain)

- special nature of cerebral BVs –> less collagen/support

23
Q

What is the definition of CHF?

A
  • failure to maintain adequate circulation due to decreased CO
  • ischaemia in front (arterial side); retention at venous side
  • “failure as a pump”
24
Q

What is CHF the end result of?

A
  • IHD
  • HTN
  • valve disorders
  • etc
25
Q

What is diastolic vs. systolic failure?

A

Systolic:

  • heart unable to properly contract –> decr. CO
  • IHD, HTN

Diastolic:

  • heart unable to properly relax/fill
  • hypertrophy, fibrosis
26
Q

What is high output cardiac failure?

A
  • normal heart but significantly increased demand
  • severe anemia, hyperthyroidism, etc
  • heart cannot cope with increased demand
27
Q

What are the Sx. of CHF?

A

Forward failure:
-failiure to maintain CO (ischaemia - arterial side)

Backward failure:

  • failure to relax
  • need increased filling pressure to maintain CO

Congestive failure:

  • fluid retention (L/R)
  • increased venous pressure
  • L - side = pulm oedema
  • R - side = systemic oedema
28
Q

What is the frank starling mechanism?

A
  • more stretch = more contraction
  • BUT eventually leads to increased ischaemia as more contraction requires more O2 (which is already low in the case of chronic IHD –> severe ischaemia)
  • initial compensation due to compensatroy increased contraction (only temporary before O2 demand is too much - ischaemic damage)
29
Q

What are the neuro-hormal mechanisms that work to maintain circulation in the face of CHF?

A
  1. vasoconstrictors (norepinephrine)
  2. RAAS
    - fluid retention
  3. Atrial natriuretic peptide
    - released from heart
    - diuresis (opposite to RAAS)
30
Q

What are the 2 types of compensatory hypertrophy of heart in CHF?

A
  1. pressure overload hypertrophy
    - concentric thickening of ventricular wall
    - thickened wall
    - normal volume
  2. volume overload hypertrophy
    - diliation of chamber itself (markedly increased volume)
    - wall may be thick/thin
31
Q

Outline RAAS as a compensatory mechanism in heart failure

A
  • renin released by endocrine cells in juxtaglomerular apparatus in kidneys in response to low BP/GFR
  • renin goes to liver where it converts angiotensinogin –> angiotensin I
  • AT I goes to lungs where ACE converts it to AT II
  • AT II causes vasoconstriction which in itself increases BP
  • AT II also stimulates adrenal glands to release aldosterone
  • Aldosterone stimulates sodium (+ thus water) reabsorption in DCT –> increased blood volume/pressure
  • ANP = negative feedback loop (*inhibits aldost. release/action thus decreasing fluid retention)
32
Q

What is the pathogenesis of SOB, weakness and anxiety in CHF?

A

-low CO + tissue perfusion

33
Q

What is acute heart failure caused by?

A

MI (sudden)

34
Q

What are the radiological signs of CHF?

A

A - alveolar bat wings
B - kerley B lines (interstitial oedema)
C - cardiomegaly (incr. L- heart border = L-sided failure and same goes for RHF)
D - dilated upper lobe vessels
E - pleural effusions and pulmonary oedema

35
Q

What are “heart-failure cells” and what does it do to the lung appearance?

A

-hemosiderin in macrophages –> result from increased pulm pressure leading to breakage of capillaries with RBC leakage into alveoli –> RBCs broken down by macrophages –> macrophages retain hemosiderin within alveoli

BROWN INDURATION OF LUNG

36
Q

True or False?

Nutmeg liver is due to congestion around portal triads in liver in RHF

A

False

-due to congestion around CENTRAL VEINS

37
Q

What are the symptoms of LHF?

A

-exertional dyspnoea** (MOST IMP.)
-PND/orthopnoea
-tachcardia
-fatigue
-cyanosis
Pulmonary congestion:
-cough
-crackles
-wheezes
-blood-tinged sputum
-tachpnoea

38
Q

What are the symptoms of RHF?

A

(COR PULMONALE)

  • ascites/sacral oedema
  • dependent (pedal) oedema
  • fatigue
  • hepatosplenomegaly
  • weight gain
  • anorexia/complaints of GI distress
  • raised JVP
  • may be secondary to secondary pulmonary problems or LHF

Pathology Term 4 (6 decks)

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