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Year 1 - Term 2: Carriage of Oxygen > CoO PBL Condtions > Flashcards

Flashcards in CoO PBL Condtions Deck (54)
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1

 What is the SAN innervated by?

 - Parasympathetic vagal fibres inhibit K+ channel closure via muscarinic cells - Sympathetic cadiac plexus fibres increase K+ channel closure in beta-adrenoreceptors

2

 How long should PR interval last?How long should the QRS complex last? 

 120-200ms<100ms

3

 What causes:The P wave?The QRS complex?The T wave?

  Atrial depolarisationVentricular depolarisationDifferences in time of ventricle repolarisation

4

 What are the ECG leads?

 6 Limb leads: I, II, III, aVR, aVL, aVF6 Chest leads: V1, V2, V3, V4, V5, V6

5

 What would you see on an ECG of AF?

 No P wave on II or aVRIrregularly irregular QRS complexHigh heart rateIrregular R-R intervals

6

AFDefinitionRisk FactorsPathophysiologySigns & SymptomsDifferentialTreatement

 Definition: Abnormal heart rhythm characterised by rapid and irregular beatingRisk factors: (CHA2DS2-VASc score) CAD, Hypertension, Age, Diabetes, Stroke (prior), MI, Heart failure, Valvular disease, Thyroid disorders, GeneticsPathophysiology: anatomically and histologically abnormal atria as a result of underlying heart disease. Progressive atrial fibrosis causes dilation and inflammation causes difference in refractory periods and promotes electrical re-entry.  Multiple wavelets. S&S: palpitations, dizziness, SoB, swelling, fatigueDifferential: atrial flutter (saw tooth waves), Wolff-Parkinson-White Syndrome, atrial tachycardiaTreatment: Rate control: beta blockers (atenolol, bisoprolol), non-dihydropyridine CCB (diltiazem), cardiac glycosides (digoxin - if sedentry), amiodrine can be used if all others inaffective. Cardioversion: electrical shock, or e.g. amiodrone. Surgery: Ablation/maze proceedure, need pacemaker afterwards 

7

 Why are patients with AF commonly placed on anticoagulants?

 Atria do not depolarise/contract in coordinated way. Blood pools in atria -> thrombus formation -> in circulation -> enters brain -> stroke or e.g. pulmonary embolism in lungs

8

 What is alfuzosin and how does it work? 

 Antagonist of alpha-1 adrenergic receptor (GPCR), relaces muscles in prostate and bladder neck, used to treat BPH

9

 What happens is the baroreceptors are not stretched enough?

 Decrease in AP number and rate -> CN IX and X afferents -> NTS -> projects to:1. Nucleus ambiguus: cardioinhibitory centre is inhibited = decreases parasympathetic vagal output to SAN 2. Vasomotor sensor in rostral venterolateral medulla -> sympathetic output increases via: lateral reticulospinal tract to preganglionic neurons of sympathetic nervous system in intermediate part of thoracolumbar ventral horn -> postganglionic neurons to vasoconstrict arteriole SM via NA on alpha-1 adrenoreceptors -> raised TPR which increases BP

10

 What happen if baroreceptors are stretched too much?

 Nucleuus ambigious cardioinhibitory centre increases parasympatheric vagal output to SANVasomotor sensor sympathetic output is inhibited

11

 What do the adenoreceptors do:alpha-1alpha-2beta-1beta-2?

 contracts vascular SMpresynaptic nerve terminals, decreases NA release by negative feedback - decreases BPin heart, increases force and rate of contractionrelaxes bronchiole smooth muscle

12

 Postural HypotensionDefinitionCauseTreatment 

Definition: a fall in systolic BP of at least 20mmHG or diastolic of at least 10mmHG within 3 minutes of standing upright. Occurs predominantly by delayed constriction of lower body BVs so blood pools in legs and less is returned to heart -> reduced CO and lower arterial pressure.Cause: Hypervolemia and intravascular fluid depletion, diseases (e.g. addison's disease - not enough steroid hormone produced), diabetes, parkinson's, pheochromocytoma, atherosclerosis), medication (diuretics, sedatives, adrenergic blockers, beta blockers, nitrates, TCAs, MAOIs), autonomic disordersTreatment: Lifestyle first (water, elevate head of bed etc.), then fludrocortisone (raises BP when given with high salt intake, corticosteriod, causes kidney to retain Na and thus blood volume. If unsuccessful: midodrine (vasopressor/antihypotensive agent, raises reduced BP, alpha-1 adrenergic agonist, used for autonomic dysfunction), or droxidopa (aa precursor, prodrug to NA, cross BBB, narrows BVs and increases BP)

13

 Why might alfuzosin cause postural hypotension?

  Sympathetic NS keeps arterioles slightly contracted. Alfuzosin blocks sympthetic NS (it is an alpha-1 adrenergic receptor antagonist so decreases blood pressure by ihibiting vasoconstriction usually initated by the baroreflex upon postural change). Blood pools in lower limbs -> decreases BP

14

 How do you calculate MAP?

 MAP = DIASTOLIC + 1/3 PULSE PRESSURE (PP is SYSTOLIC - DIASTOLIC)

15

 

What is amiloride and what is it used to treat?

How does it work?

 

A potassium-sparing diuretic ofen used for hypertension and congestive heart failure. They are competitive antagonists and compete with aldosterone or block Na+ channels (ENaC). Thus Na/K sites do not work, Na+ is not reabsorbed, and K+ and H+ is not secreted.

Often used with loop diuretics that would otherwise lower K+ levels dangerously. 

16

 

What does SCNN1B encode?

 

 

Beta subunit for epithelium ENaC (heterotrimer) involved in generating APs in neurons an body fluid regulation. Strongly inhibited by amiloride.

17

 

Liddle Syndrome

Definition

Cause

Signs & Symptoms

Diagnosis

Treatment

Definition: autosomal dominant genetic disorder, early severe hypertension involving abnormal kidney function with excess Na+ reabsorption and K+ loss from renal tubule.

Cause: proline -> leucine mutation on c terminal of beta and gamma subunit of ENaC (normally transports Na into cells). It is no longer degraded by ubiquitin proteasome system becuase PY motif altered so Nedd4 no longer recognises channel). This increases ENaC activation in the CD -> "hyperaldosteronism-like state" -> increased Na and H2O reabsorption -> increased extracellular vol -> hypertension. There is excretion of K+.

Signs & Symptoms: early onset severe hypertension, hypokaleamia, metabolic alkalosis (decreased H+ conc), weakness

Diagnosis: blood test and genetic testing

Treatment: low Na diet, potassium-sparing diuretics specific for Na channel e.g. amiloride and triamterene

18

 

What would you see on a blood test of someone with Liddle Syndrome?

 

Low plasma renin and aldosterone levels

Elevated serum Na+

Elevated serum bicarbonate (low extracellular K+, so K+ leaves cells, and H+ enters, raising blood pH)

Reduced serum K+

 

19

 

What happens if there is persistant low Na in the DCT?

persistant low Na in DCT -> macula densa signals to juxtaglomerular cells -> renin released to efferent arteriole -> cleaves angiotensinogen from liver to angiotensin I -> to lungs -> cleaves by angiotensin-converting enzyme (ACE) to angiotensin II:

1) vasoconstrictor of systemic arterioles -> increases afterload, BP and GFR

2) aldosterone secretion from adrenal cortex -> acts on DCT receptors (ENaC and Na/K pump expression) and stimulates Na resorption -> H2O reabsorption -> blood volume increase -> increases preload, BP and GFR 

20

 

Describe the actions of aldosterone in the kidney

 

- Upregulation and activation of basolateral Na/K pumps

- Upregulation of ENaCs

- Increase in K+ secretion

- Increase Na reabsorption and thus H2O retention

21

 

Another name for ADH?

 

arginine vasopressin

22

 

How can hypertension lead to development of L ventricular hypertrophy?

 

Hypertension -> increased afterload -> heart works harder to eject same volume of blood in systole -> over time this may lead to thickening of myocardium

23

 

Describe transcellular pathway for Na reabsorption within the cortical and medullary tubule in kidney.

 

1) Passive Na entry into cell from tubule lumen across apical membrane via epithelial Na channels via ENaC facilitated by electrochemical gradient

2) Active extrusion of Na out of cell across basolateral membrane mediated by  Na/K ATPase pump

24

VC is a measurement of what?

FEV1 is a measurement of what?

FVC is a measurement of what?

Greatest vol of air that can be expelled from lungs after taking deepest poss breath.

Vol exhaled at end of first second of forced expiration

VC determination from max forced respiratory effort

25

What is the main muscle of respiration?

Where is the main site of airway resistance?

Diaphragm

Small bronchi and bronchioles

26

Describe the function of the alpha-1 antitrypsin enzyme in the lung

It's a protease inhibitor - proteases are released by inflammatory cells which break down elastin. Lack of the enzyme may lead to emphysema.

27

What types of WBC are found in alveoli?

Neutrophils, eosinophils. + mast cells.

28

Describe the airway tree

Mouth and nose -> parynx -> trachea -> main bronchus -> lobar bronchi -> segmental bronchi -> conducting bronchioles ->  terminal bronchioles -> respiratory bronchioles -> alveolar ducts -> alveolar sacs

Divides 23 times

29

What muscles are involved in:

a) quiet inspiration

b) quiet expiration

c) deep inspiration

d) deep expiration

a) dipahragm, external intercostals

b) passive (recoil)

c) scalene, SCM, pectoralis minor

d) interosseus part of internal intercostals, abdominal, serratus posterior inferior

30

How can you distinguish obstructive and restrictive lung disorders from FEV1, FVC and the FEV1/FVC ratio?

FEV1: reduced (<80%) in O and R

FVC: reduced but to a lesser extent in O than R (<80%)

FEV1/FVC: Reduced (<0.7) in O, normal (>0.7) in R

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