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Cardiorespiratory 2 > Before The Exam > Flashcards

Before The Exam Flashcards

1
Q

How do you work out the ESR

A

age (+10 if female)/2

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2
Q

what are the sings of anaemia

A 
pallor
retinal haemorrhages
cardiac failure 
systolic murmur 
bounding pulse
rapid heart rate
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3
Q

what is the ferric symbol and what is the ferrous symbol

A

ferric = Fe3+
ferrous = fe2+
ferric reductase causes ferric to be converted to ferrous in the gut

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4
Q

what happens if there is bundle branch block

A
  • prolonged QRS

- loss of synchronic

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5
Q

what does a VSD lead do

A

left to right shunting

pulmonary hypertension

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6
Q

what does an ASD lead to

A

left to right shunting
pulmonary hypertension
right ventricular hypertrophy

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7
Q

define megaloblastic anaemia

A

is macrocytic anaemia that results from inhibition of DNA synthesis during red blood cell production

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8
Q

describe the features of pernicious anaemia and what causes it

A
  • An autoimmune disorder
  • Incidence is 1-2% in population > 60 years
  • F > M
  • Associated with fair hair, blue eyes, blood group A
  • Due to an Autoantibody against parietal cells and intrinsic factor (IF)
  • Leads to gastric atrophy, ↓ acid + ↓ IF secretion
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9
Q

what do the lab tests show for pernicious anaemia

A
  • microcytic anaemia
  • hypersegemented neutrophils
  • decreased serum B12
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10
Q

what can long standing haemolysis cause

A

gall stones

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11
Q

what is the presentation of haemolytic anaemia

A
  • Pallor and signs/symptoms of anaemia
  • Jaundice
  • Gallstones
  • Splenomegaly
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12
Q

what is the difference between hereditary spherocytosis and GP6D deficiency

A

Hereditary spherocytosis is a autosomal domintant condution whereas GP6D is an a X linked condition

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13
Q

what is the differnece between pituitary macroadenoma and pitutiary microadneoma

A

macroadenoma is greater than 10mm

whereas microadenoma is less than 10mm

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14
Q

what does PTH do to osteoblasts

A

it inhibits osteoblasts

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15
Q

what does PTH do to calcium absorption in the gut

A
  • it increases calcium reabsorption from the gut but not directly, it uses vitamin D
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16
Q

PTH does not….

A

facilitate phosphate reabsorption

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17
Q

what are the causes of hypopituitism

A
  • pituitary radiotherapy
  • macro adenoma
  • empty sella
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18
Q

what treatment is not used in osteoporosis

A

FGF-23

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19
Q

what does FGF=23 do

A

= FGF23 this is a phosphatonin - a hromone that reduces the serum phosphate levels

  • it is secreted in osteocytes in response to 1,25-dihydroxyvtiamin D3
  • its action is to induce phosphaturia in the kdineys by increasing renal loss of phsophate and to inhibit 1 alpha hydroxylase whcih is needed to form 1,25-dihydroxyvitamin D3
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20
Q

In angina what causes an increase in oxygen demand and what can cause a decrease in oxygen supply

A

increase in oxygen demand

  • hypertrophy
  • stenosis
  • pulmonary hypertension
  • hypertension

decrease in supply

  • atheroscerlosis
  • severe anaemia
  • regurgitation
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21
Q

what is another pathway by which VWF carries out its role

A
  • 2nd pathway of activation by agonists interaction on membrane surface receptors and G protein activation of phopholipase C. – further calcium release – stimulate contractile system – liberation of Arachidonic Acid and further generation of TXA2
  • Flip fop of membrane charge – negative charged moieties onto outer surface – procoagulant
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22
Q

what does antithrombin inhibit

A

major inhibitor of thrombin and Xa

• also inhibits VII, IX, XI

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23
Q

what does protein C do in clotting

A
  • serine protease
  • inactivates Va and VIIIa
  • Protein S
  • cofactor for Activated Protein C (APC)
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24
Q

what are emerging risk factors for atherosclerosis

A
  • Increased Homocysteine (B6, B12 & folic acid deficiencies)
  • Increase oxidant stress
  • Lipoprotein (a) - (LDL + extra apolipoprotein)- more firmly retained in arterial wall
  • Infection (Chlamydia pneumoniae)- inflammation of endothelium
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25
Q

Name the 4 possible causes of hypertension

A
  1. Overactivity of the sympathetic nervous system
  2. Impaired production of nitric oxide
  3. Elevated renin release
  4. Reduced atrial natriuretic peptide release
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26
Q

How do you work out blood pressure

A

Blood pressure P = Cardiac output x SVR

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27
Q

what causes the Link between obesity and primary hypertension

A

1)
- Obese individuals have high levels of leptin but often have a decreased sensitivity to leptin and thus their ‘ponderostat’ control is set too high.
- The high levels of leptin produce overstimulation of the sympathetic nervous system, especially the supply to the kidney.
- This may directly stimulate excess renin release.
2)
- Obesity is associated with hyperinsulinaemia and insulin resistance.
- hyperinsulinaemia can damaging endothelial walls and decrease nitric oxide production, thus increasing SVR and inducing hypertension

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28
Q

what investigations initially should you do for pulmonary embolism

A
  1. ECG – sinus tachycardia, right heart strain, T-wave inversion on anterior leads.
  2. CXR – often normal, focal oligaemia, peripheral wedge shaped density above diaphragm, small pleural effusion
  3. Arterial blood gases – often hypoxia, low CO2, but may be normal
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29
Q

what are the causes of dilated cardiomyopathy

A
  • idiopathic
  • familial

Inflammatory

  • infectious (especially viral)
  • non infectious
  • connective tissue disorders
  • permpartum cardiomyopathy
  • Sarcodosis

Toxic

  • chronic alcohol consumption
  • chemotherapeutic agents

metabolic

  • hypothyroidism
  • chronic hypocalcameia

neuromuscular
- muscular or myotonic dystrophy

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30
Q

what are the signs and symptoms of dilated cardiomyopathy

A
  • Decreased cardiac output – tiredness and fatigue
  • Pulmonary oedema – Dyspnoea/Crackles
  • Ascites and peripheral oedema (in legs, ankles)
  • Enlarged heart – leftward displacement of apical beat and possibly a third heart sound (indicates poor systolic function)
  • Mitral regurgitation – regurgitation of blood back into the left atrium
  • Palpitations – this is caused by arrhythmias
31
Q

what are the symptoms of hypertrophic cardiomyopathy

A

There is wide variation in the symptoms of HCM, with some people having few or no symptoms, to people who have very severe symptoms
• Palpitations – caused by arrhythmias.
• Chest pain – reduced oxygen levels getting to the heart.
• Dizziness or fainting – reduced oxygen levels or blood flow to the brain.
• Breathlessness (or dyspnoea) – pulmonary oedema, making it harder to breathe.

32
Q

what are signs and symptoms of restrictive cardiomyopathy

A
  • Decreased cardiac output - fatigue (tiredness)
  • Systemic congestion
  • Jugular venous distension
  • Peripheral oedema
  • Arrhythmias - Palpitations
  • Possible conduction block
  • Signs of congestive heart failure may also be present e.g. pulmonary crackles etc.
33
Q

describe the T cell response to asthma

A
  • Dendritic cell causes activation of TH2 cell
  • TH2 cells are activated : there Central role is Release inflammatory mediators:
  • interleukin-4 (IL-4) and IL-13 = Stimulates B cells to synthesize IgE
  • IL-5 = Eosinophil activation
  • IL-9 = mast cell proliferation – this causes an increased histamine production and further activation of mast cells
34
Q

How is COPD caused

A
  • Cigarette smoke (major risk factor) = irritates & activates epithelial cells & macrophages → inflammatory mediators

Macrophages release CXCL8
= chemokine = attracts neutrophils

Epithelial cells release CXCL9 & CXCL10 = chemokine = attracts T helper 1 (TH1) cells and type 1 cytotoxic T (TC1) cells

TC1 & neutrophils → Proteases (e.g. metalloproteinase 9 (MMP9)leads to = elastin degradation

Neutrophil elastase leads to = mucus hypersecretion.

Epithelial cells & macrophages → transforming growth factor-β (TGFβ) = stimulates fibroblast proliferation = fibrosis in the small airways

35
Q

what are the clinical signs of COPD

A
  • Shortness of breath
  • Chronic cough
  • Phlegm
  • Wheezing
  • Chest tightness
  • Respiratory infection
36
Q

what are the symptoms of idiopathic pulmonary fibrosis

A
    • difficult to distinguish
  • Extertional dyspneoa
  • Clubbing
  • Dry cough
37
Q

how to you diagnose sarcoidosis

A
  • Info from the patient and
    Clinicoradiographic data:
  • Bilateral hilar adenopathy on the chest radiograph
  • Lofgren syndrome (erythema nodosum skin rash + bilateral hilar adenopathy on chest radiograph +/- fever and arthritis)
  • Diagnosis possible versus idiopathic granulomas – for example one organ has granulomas if there is more than one granuloma then diagnosis is more likely
38
Q

what are the major symptoms of a common cold

A

Rhinorrhoea (excess mucus filling in the nasal cavity) and nasal obstruction (mucosal lining) – major symptoms

39
Q

name the categories for the centor score for pharyngitis

A
  • Tonsillar exudate
  • Tender anterior cervical lymphadenopathy or lymphadenitis
  • History of fever greater than 38 degrees
  • No cough
40
Q

name the categories for the FeverPain score for pharnygitis

A
  • If the person has fever above 38 degrees
  • Purulence
  • Attend within 3 days or less
  • Severly inflamed tonsils
  • No cough or coryza
41
Q

what are the signs of hypovalemic shock

A
  • confusion / anxiety,
  • cold
  • clammy skin (sympathetic nervous system turns of taps to the skin),
  • low BP,
  • high heart rate,
  • slow capillary refill,
  • greyish pallor,
  • oliguria,
  • absent bowel sounds.
  • Reduction in blood flow to the kidney – not the first line of defence
42
Q

what are the symptoms of patients with cardiogenic shock

A

present with the constellation of symptoms of acute cardiac ischemia
- chest pain
- shortness of breath
- diaphoresis
- nausea
- vomiting
Patients experiencing cardiogenic shock also may present with pulmonary edema, acute circulatory collapse, and presyncopal or syncopal symptoms.

43
Q

what are the signs of cardiogenic shock

A

ECG shows the pattern of AMI or acute coronary insufficiency
Systolic BP < 80 mm Hg *
Pulse rate is 100 per min or faster
The urinary output is low, 30 ml or less per hour
There are clinical signs of peripheral circulatory collapse

44
Q

what are the symptoms of septic (distributive shock)

A
  • low BP
  • tachycardia
  • fever - this could be absent in elderly or immunosuppressed patients
  • chills
  • rigors
  • fatigue
  • malaise
  • nausea
  • vomiting
  • difficulty breathing
  • anxiety
  • confusion
45
Q

what are the signs of obstructive shock

A
  • tachycardia and anxiety of hypovolemic shock are present.
  • chest pain
  • breath sounds are absent on the affected hemiothorax - the trachea deviates away from the affected side.
  • A pulmonary embolism* (PE) can cause obstructive shock.
46
Q

what are the clinical symptoms of hypovolaemic shock

A
  • Tachycardia,
  • Pale, Shut down
  • Sweaty, Clammy
  • Oliguria
  • Confusion
47
Q

what are the symptoms of sepsis

A
  • Temp > 38oC or < 36oC
  • HR > 90 bpm
  • RR > 20 bpm or PaCO2 < 32 mmHg
  • WBC > 12 x 109/L, or >10% band form
48
Q

what are the clinical signs for ischemic myocardial injury

A 
–	Chest pain
–	 4th heart sound
–	 Low grade fever
–	 Leucocytosis and raised inflammatory markers (ESR, CRP)
–	 Troponin leak
49
Q

what is the drug treatment for an NSTEMI

A
  • Aspirin and ticagrelor
  • ± GP IIb/IIIa inhibitor
  • Fondaparinux (factor Xa inhibitor)
  • Anti-ischaemic drugs (BB, nitrates)
  • Angiography ± PCI within 24-96 hrs
50
Q

how do you work out

  • vital capacity
  • end respiratory volume
  • total lung capacity
  • inspiratory capacity
  • functional residual volume
  • expiratory reserve volume
A
  • vital capacity = is calculated by adding the inspiratory reserve volume, the tidal volume and the expiratory reserve volume (IRV + VT + ERV)
  • end respiratory volume = measured, total lung capacity (TLC)
  • total lung capacity = is calculated by adding the inspiratory reserve volume, the tidal volume, the expiratory reserve volume and the residual volume (IRV + VT + ERV + RV)
  • inspiratory capacity = is calculated by adding the tidal volume and the inspiratory reserve volume (VT + IRV)
  • functional residual volume = FRC) is calculated by adding the expiratory reserve volume and the residual volume (ERV + RV)
  • expiratory reserve volume = (ERV) is a measured value and cannot be calculated
51
Q

what are the clinical findings of aortic stenosis

A
  • dyspnoea - increase in diastolic pressure in stiff non-compliant LV
  • Angina - increase in O2 demand of hypertrophied LV, thickened aortic valve as the ventricles have to generate more pressure to push blood through the valve thus is hypertrophied and it needs oxygen which the coronary cannot deliver, patietns are often quite old as have coronary disease so reduced oxygen levels
  • Syncope - either paroxysmal ventricular arrhythmias or exertional cerebral hypoperfusion, if you have aortic stenosis and you black out this is a serious sign, due to hypotension heart cannot increase blood around body
  • LVF - contractile failure as ventricle dilates
  • Sudden death - ventricular arrhythmias
52
Q

what are the signs of aortic stenosis

A

Slow rising carotid pulse
S4 ± ejection click
Ejection systolic murmur

53
Q

what are the clinical signs of aortic regurgitation

A
  • Rapidly rising carotid pulse - vigorous ejection of volume loaded LV
  • Early diastolic murmur - aortic backflow (left sternal edge)
  • Ejection murmur - turbulent ejection from volume loaded LV (left sternal edge)
54
Q

what are the symptoms of mitral stenosis

A

Dyspnoea, orthopnoea - increased left atrial pressure

RV failure- passive consequence of increased left atrial pressure and reactive pulmonary vasoconstriction

Palpitations atrial fibrillation

Systemic emboli - static blood within dilated fibrillating left atrium predisposes to thrombosis

55
Q

what are the signs of mitral stenosis

A

Pulse - AF

Auscultation (heart)- loud S1, opening snap, mid-diastolic rumble, ± pre-systolic murmur (SR only)

Volume overload - increased JVP, basal creps, ankle oedema

56
Q

what are the signs of mitral regurgitation

A

Pulse - SR/AF

Auscultation (heart) - Pansystolic murmur S3

Volume overload -increased JVP, basal creps, ankle oedema

57
Q

what are the signs of lacunar strokes

A
  • Well defined deficits are present but cortical infarct signs (such as aphasia, neglect, and visual field defects) are always absent
58
Q

how do you treat atrial fibrillation thus lowering the risk of stroke

A

Give Aspirin for healthy patients < 65 years

Give Warfarin for patients > 65 years or having other stroke risk factors

59
Q

describe hypersensitivity type 1

A
  • Mast cell activation.
  • Release of mediators: Histamine, leukotrienes (& prostaglandins).
  • IgE mediated
60
Q

describe the differnet types of hypersenstivity

A

type 1
- IgE and mast cells - allergies, astham

type 2
- IgG and IgM and complement, graves, rheumatic fever

type 3

  • IgG
  • complement
  • neutrophils
  • e.g. lupus

type 4

  • t cells
  • e..g tb, hasmitos thyroditis, coeliacs

type 5

  • autoimmune, IgG, IgM
  • graves and myansthesia gravis
61
Q

what are the common causes of type 1 respiratory failure

A

 Ventilation/Perfusion (V/Q) mismatch
 Shunting of blood across lungs
 Poor gas exchange (alveoli filled with fluid eg in pneumonia)
 Decreased minute ventilation (MV) relative to demand
 Increased dead space ventilation (less gas to alveoli)

62
Q

name 4 things that can happen when NO is impaired

A
  1. Vasoconstriction (e.g., coronary vasospasm, elevated systemic vascular resistance, hypertension)
  2. Thrombosis due to platelet aggregation and adhesion to vascular endothelium
  3. Inflammation due to upregulation of leukocyte and endothelial adhesion molecules
  4. Vascular hypertrophy and stenosis
63
Q

what is the VO2

A

the rate of oxygen uptake by skeletal muscle

64
Q

How do you work out MCV

A

haematocrit/ red cell count

65
Q

Why is vitamin C given in order to help iron absorption

A

Iron can only be absorbed as the ferrous ion (1 mark). Vitamin C is a reducing agent and will reduce dietary ferric iron to ferrous iron to improve absorption (1 mark)

66
Q

what can cause a D dimer test other than a clot

A

Increased fibrin formation may be caused by VTE but also by cancer, infection, inflammation, post-op, pregnancy ( 1 mark)

67
Q

PE symtpoms

A

= chest pain pleuripotic

  • dyspnea
  • shortness of breath
68
Q

what is a tuberculin

A

Tuberculin is the name given to purified protein derivative (1/2 mark) (PPD) extracts of Mycobacterium tuberculosis, M. bovis, or M. avium (1/2 mark any one)

69
Q

2) Name two consequences of hyperthyroidism on glucose metabolism. [2
marks]

A

Hyperthyroidism leads to Insulin resistance [1], mainly associated with increased
hepatic gluconeogenesis [1].

70
Q

Explain why the thyroid gland is enlarged in Hashimoto thyroiditis

A

Thyroid enlargement is induced by an inflammatory infiltrate of immunocytes that
replace the parenchyma and subsequent fibrosis [1]

71
Q

explain how an insulin stress test works

A

(i) Growth hormone levels are pulsatile and almost undetectable for most of the
day and so growth hormone levels are measured by their response to stimulation
[1 mark]
(ii) Gold standard is insulin-induced hypoglycaemia [1 mark]
Blood is taken for growth hormone, cortisol and glucose and then fast-acting
insulin is injected intravenously. Blood is taken again for growth hormone, cortisol
and glucose after 30, 45, 60, 90 and 120 minutes. [1mark]

72
Q

What is NSILA and which hormone accounts for it? [2 marks]

A

NSILA: nonsuppressible insulin-like activity. [1 mark]

The insulin-like biological effects of IGFs accounts for NSILA [1 mark]

73
Q

Left sided heart failure causes…

A

Pulmonary oedema whereas right sided heart failure causes peripherla oedema

Cardiorespiratory 2 (43 decks)

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