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Pathology Term 4 > Week 4 - CHF > Flashcards

Week 4 - CHF Flashcards

HTN, Cor Pulmonale (38 cards)

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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?

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A
  • asymptomatic (compensated)

- hepatic congestion (nutmeg) –> Cor pulmonale

17
Q

What are the 2 types of microangiopathy?

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

2. hyperplastic arteriolosclerosis –> SMC proliferation (HTN)

18
Q

What are the 4 grades of hypertensive retinopathy?

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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?

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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?

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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?

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A

> 200/120mmHg

22
Q

Where is the commonest site of BV rupture and why?

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A
  • cerebral vessles (brain)

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

23
Q

What is the definition of CHF?

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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?

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A
  • IHD
  • HTN
  • valve disorders
  • etc
25
What is diastolic vs. systolic failure?
Systolic: - heart unable to properly contract --> decr. CO - IHD, HTN Diastolic: - heart unable to properly relax/fill - hypertrophy, fibrosis
26
What is high output cardiac failure?
- normal heart but significantly increased demand - severe anemia, hyperthyroidism, etc - heart cannot cope with increased demand
27
What are the Sx. of CHF?
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
What is the frank starling mechanism?
- 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
What are the neuro-hormal mechanisms that work to maintain circulation in the face of CHF?
1. vasoconstrictors (norepinephrine) 2. RAAS - fluid retention 3. Atrial natriuretic peptide - released from heart - diuresis (opposite to RAAS)
30
What are the 2 types of compensatory hypertrophy of heart in CHF?
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
Outline RAAS as a compensatory mechanism in heart failure
- 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
What is the pathogenesis of SOB, weakness and anxiety in CHF?
-low CO + tissue perfusion
33
What is acute heart failure caused by?
MI (sudden)
34
What are the radiological signs of CHF?
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
What are "heart-failure cells" and what does it do to the lung appearance?
-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
True or False? | Nutmeg liver is due to congestion around portal triads in liver in RHF
False | -due to congestion around CENTRAL VEINS
37
What are the symptoms of LHF?
-exertional dyspnoea** (MOST IMP.) -PND/orthopnoea -tachcardia -fatigue -cyanosis Pulmonary congestion: -cough -crackles -wheezes -blood-tinged sputum -tachpnoea
38
What are the symptoms of RHF?
(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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