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Medicine > Case 3 > Flashcards

Case 3 Flashcards

1
Q

What would you prescribe to a 52 year old Caucasian male with hypertension?

A

ACE inhibitors or a low cost Angiotensin II receptor blockers

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2
Q

What would you prescribe to a 70 year old Caucasian woman with hypertension?

A

Calcium channel blockers (CCB)

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3
Q

A patient with hypertension has been on ACE inhibitors for 3 months and has still not improved in their condition. What is your next step?

A

Prescribe CCB’s along with the ACE inhibitors.

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4
Q

What would you prescribe to someone with hypertension but also an intolerance to ACE inhibitors and low cost ARBs?

A

Beta blockers

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5
Q

What would you prescribe to a young woman (who can still have children) that has been diagnosed with hypertension?

A

Beta blockers

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6
Q

If a patient with hypertension is not improving after being prescribed an ACE inhibitor and a CCB, the next step is to seek expert advice and monitor their treatment annually. True/False?

A

False

The next step (step 3) is to prescribe a thiazide diuretic drug

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7
Q

When does Hypertension become resistant?

A

When ACE inhibitors/ ARBs, CCBs and Thiazide diuretic drugs do not reduce the hypertension.

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8
Q

What should be prescribed to a patient with resistant hypertension and low blood potassium?

A

Low dose spironolactone diuretic

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9
Q

What should be prescribed to a patient with resistant hypertension and high blood potassium?

A

Higher dose spironolactone diuretic

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10
Q

What is prescribed if spironolactone diuretic drug does not work?

A

Alpha or beta blockers

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11
Q

What is the final step in treatment for hypertension (if the drugs do not work)?

A

Seeking expert advice and monitoring annually

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12
Q

What would you prescribe to a 48 year old male of afro-Caribbean descent with hypertension?

A

CCB

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13
Q

What would you prescribe to a 60 year old male of afro-Caribbean descent with hypertension?

A

CCB and ARB/ Thiazide diuretic

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14
Q

What do CCBs do?

A

Inhibit the influx of calcium ions

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15
Q

Describe the locations where CCBs act and their effect on these areas

A

myocardial muscle - inhibit contractility
myocardial conducting system – inhibit formation and propagation of depolarisation
vascular smooth muscle - coronary or systemic vascular tone reduced, allowing vasodilation

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16
Q

Give an example of a CCB

A

Amlodipine

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17
Q

What does ‘contraindication’ of a drug mean?

A

Contraindication is a warning explaining when a drug may cause harm. A relative contraindication implies there is a risk in giving the medication in a certain circumstance.

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18
Q

If a CCB is taken orally, what is its expected bioavailability?

A

60%

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19
Q

What is the half life of amlodipine?

A

30-50 hours

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20
Q

How long does amlodipine stay in the body plasma?

A

It remains in steady-state plasma concentrations for up to 7 to 8 days (daily dosing)

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21
Q

Where is amlodipine metabolised?

A

In the liver by Cytochrome P450 enzymes

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22
Q

Does renal function affect amlodipine elimination?

A

No

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23
Q

Give an example of an ACE inhibitor

A

Lisinopril

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24
Q

What do ACE inhibitors do?

A

Inhibit the angiotensin-converting enzyme in the renin-angiotensin system

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25
Q

What is the bioavailability of lisinopril that is taken orally?

A

25%

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26
Q

When does the peak plasma concentration of lisinopril occur?

A

4-8 hours

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27
Q

What is the half life of lisinopril?

A

12 hours

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28
Q

Where is lisinopril metabolised?

A

Trick question

It is not metabolised in the liver because it is water soluble and undergoes renal excretion without change

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29
Q

Does renal function affect ACE inhibitors?

A

Yes, if renal impairment: use with caution, starting with low dose, and adjust according to response. Hyperkalaemia and other side- effects of ACE inhibitors are more common in those with impaired renal function and the dose may need to be reduced.

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30
Q

Give an example of an ARB

A

Losartan

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31
Q

How do ARBs work?

A

Selective competitive blockers of angiotensin II at the AT1 receptor

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32
Q

What is the bioavailability of losartan if taken orally?

A

32%

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33
Q

Describe the metabolism of losartan

A

Undergoes 1st pass metabolism - 14% becomes an active metabolite which is more potent, non-competitive and longer acting.
Then it is metabolised by Cytochrome P450 enzymes.

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34
Q

What is the half life of loartan metabolite?

A

3-9 hours

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35
Q

What is the terminal half life of losartan?

A

2 hours

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36
Q

Is losartan protein binding?

A

Yes, binds to 98% of plasma proteins

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37
Q

Where is losartan lost?

A

Bile and urine

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38
Q

Give an example of a Thiazide diuretic drug

A

indapamide

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39
Q

How do Thiazide diuretic drugs work?

A

Inhibits reabsorption of Na+ and Cl− from the distal convoluted tubules by blocking the Na+-Cl− symporter.
At lower doses vasodilatation is more prominent than diuresis.

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40
Q

How is indapamide taken?

A

Orally

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41
Q

Indapamide is 75% protein plasma bound. True/False?

A

True

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42
Q

What is stage 1 Hypertension?

A

In the clinic, BP is 140/90 or higher
Followed by an ambulatory recording of 135/85 or higher and have one of the following
•target organ damage
•established cardiovascular disease
•renal disease
•diabetes
•10-year cardiovascular risk equivalent to 20% or greater.

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43
Q

Why might someone have a higher BP in the clinic than in the ambulance?

A

Stress

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44
Q

What is stage 2 Hypertension?

A

A clinic BP of 160/100 or higher

Followed by BP of 150/95 or higher in the ambulance

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45
Q

If a clinic BP reading is 180/110 or higher, what is the next step?

A

Treatment immediately

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46
Q

What are risk factors for hypertension?

A 
Age
Gender/Sex
Smoking
Postcode
Medical history
Family history
Rheumatoid arthritis
Cholesterol/HDL ratio
BP
BP Treatment
Diabetes
Ethnicity
BMI
Atrial Fibrillation
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47
Q

What is the difference between essential/primary hypertension and secondary hypertension?

A

Primary hypertension has no clear cause and develops gradually over the years and with increasing age. In young patients under 40, usually due to high cardiac output, and with older patients it’s because of stiff arteries (high peripheral resistance).
Whereas secondary hypertension happens as a result of an underlying condition, such as…
-Obstructive sleep apnea
-Kidney problems
-Adrenal gland tumors
-Thyroid problems
-Certain defects you’re born with (congenital) in blood vessels
Secondary hypertension can also occur from taking drugs like…
-birth control pills
-cold remedies
-decongestants
-over-the-counter pain relievers
-some prescription drugs
-Illegal drugs such as cocaine and amphetamines

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48
Q

What is arteriosclerosis?

A

The thickening, hardening, and loss of elasticity of small arteries which gradually restricts the blood flow to tissues.

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49
Q

What is atherosclerosis?

A

Development of fatty plaques and cholesterol in the wall of arteries as part of an inflammatory response. It is not limited to small arteries.

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50
Q

How can Hypertension lead to congestive heart failure?

A

-Increase in afterload (pressure heart has to overcome so blood will pump)
-Systolic dysfunction = Congestive heart failure
OR
-Left Ventricular Hypertrophy
-Diastolic dysfunction = Congestive heart failure

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51
Q

How can Hypertension lead to Myocardial Infarction?

A

-Increase in afterload
-Increase in myocardial oxygen demand (O2 required by heart) = Angina which will become MI if left untreated
OR
-Arterial damage
-Accelerated atherosclerosis
-Decrease in myocardial oxygen supply = Angina

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52
Q

How can Hypertension lead to aortic aneurysm?

A

-Arterial damage
-Accelerated atherosclerosis of aorta = aortic aneurysm
OR
-Weakened vessel wall of aorta = aortic aneurysm

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53
Q

How can Hypertension lead to a stroke?

A

-Arterial damage
-Accelerated atherosclerosis of carotid/cerebral arteries
-Thrombosis (coagulation/clotting of blood) and atheroemboli (blood clot of cholesterol) = Stroke
OR
-Weakened vessel wall
-Cerebral haemorrhage = Stroke

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54
Q

How can Hypertension lead to kidney failure?

A
  • Arterial damage

- Weakened vessel wall of arteries supplying oxygen to kidneys = Kidney failure

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55
Q

How can Hypertension lead to retinopathy?

A
  • Arterial damage

- Weakened vessel wall of arteries supplying to eyes = Retinopathy (damage to retina)

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56
Q

Name all the types of shock

A
  • Hypovolaemic
  • Anaphylactic
  • Septic
  • Cardiogenic
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57
Q

What is hypovolaemic shock?

A

Too much blood has been lost, and the heart cannot pump a sufficient amount of blood to the rest of the body. Can lead to organ failure.

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58
Q

What is anaphylactic shock?

A

Shock in response to allergin exposure

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59
Q

What is septic shock?

A

Can happen during sepsis - when organs are damaged in response to infection. This leads to low BP.

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60
Q

What is cariogenic shock?

A

When heart cannot pump enough blood around body to meet needs.

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61
Q

What is ‘shock’?

A

Decreased tissue perfusion, which leads to arterial systolic, diastolic and pulse pressures all reducing.

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62
Q

Describe what causes hypovolaemic shock

A

-Blood loss from body
-Decreased blood volume
-Decreased preload
-Heart cannot pump enough blood to rest of body
=lower SV = lower CO = low tissue perfusion

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63
Q

Describe what causes cardiogenic shock

A

Cardiac tamponade
-Pericardium is penetrated and fluid can enter
-Build up of fluid (pericarditis)
-Fluid accumulates around heart
-Heart is compressed and cannot fill up normally
Pulmonary embolism
-Blood clot lodged in pulmonary arteries
-Blood can’t flow into lungs
-Obstructs outflow from heart
Mechanical failure
-MI (Myocardial Infarction), heart cannot generate enough pressure to push blood
Electrical failure
-Complete heart block, signal generated in SA node not propagated in ventricles
-Ventricles beat at own rate
-Insufficient rate to maintain MAP

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64
Q

Describe what causes septic shock

A

-Bacterial infections increases expression of iNOS (NO producing enzyme)
-Overproduction of NO
NO is a vasodilator = vascular smooth muscle relaxes and BP falls

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65
Q

What are the symptoms of shock?

A
  • Rapid weak pulse (low force of contraction, body responding to sudden drop in BP)
  • Skin pale, cold and moist (activation of sympathetic nerves)
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66
Q

The body responds to a haemorrhage by switching on the sympathetic nervous system. Describe what happens after.

A

-The SA node increases firing
-More forceful contractions
-Increase in HR
-Vasoconstriction of arterioles and veins
-Blood pushed from venous to arteriole systems = BP increases
AND
-ADH = vasoconstriction

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67
Q

What are the effects of decreased renal perfusion?

A

-Renin-Angiotensin system is stimulated
-Angiotensin II is formed and constricts blood vessels, releases ADH, induces LVH
= Increase in CO, venous return, blood volume and decrease in urine formation

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68
Q

What happens if too much blood has been lost after hypovolaemic shock?

A
  • Body enters refractory shock (irreversible and results in death)
  • The sympathetic NS is switched off, and the Parasympathetic NS is switched on.
  • HR begins to reduce
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69
Q

What happens if too much blood has been lost after hypovolaemic shock?

A
  • Body enters refractory shock (irreversible and results in death) and cannot restore MAP
  • The sympathetic NS is switched off, and the Parasympathetic NS is switched on.
  • HR begins to reduce
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70
Q

Describe what leads to a positive outcome after hypovolaemic shock

A
  • MAP drops
  • Sympathetic nerves switch on
  • Boosting of circulatory blood volume
  • Gradual restoring of MAP
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71
Q

How do haemorrhages affect auto transfusion?

A
  • Blood loss means less force pushing blood out of capillaries into tissues (decrease in hydrostatic pressure)
  • Still the same amount of plasma proteins however, so oncotic pressure stays the same
  • Same amount of blood coming back into capillaries
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72
Q

What is a protective physiological mechanism during a haemorrhage?

A

As water moves in and out of capillaries, concentration of protein in tissue fluid will increase = acts as break. Only a certain amount of fluid can move from tissues back into circulation before oncotic pressure in tissues increases and movement of fluid back into blood stream slows. In blood loss, the circulating blood volume can be boosted from net movement of water from tissue fluid back into bloodstream. Emergency, takes half hour – but can save life.
* up to 500ml volume added to the plasma

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73
Q

What is the name of the plasma protein?

A

Albumin

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74
Q

Describe the protective mechanism that occurs when blood vessel walls are damaged

A
  • Platelets are exposed to collagen (component of cell wall)
  • Platelets are activated
  • Stick together to form a ‘plug’ (1st stage of clot formation)
  • There is also a release of vasoconstrictor molecules (override vasodilation)
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75
Q

What happens in response to a haemorrhage to stop blood loss?

A
  • Sympathetic nerves synapse onto vascular smooth muscle and switch on
  • If alpha 1 receptor mediated vascular smooth muscle cells – increase in vasoconstriction
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76
Q

What is the purpose of clotting?

A

Shutting down of blood vessels around cut, temporary stopping of blood flowing to damaged area = reduce blood loss

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77
Q

What test should be done for someone at risk of developing Angina or MI?

A

Arrange for a 12-lead electrocardiograph to be performed.

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78
Q

What test should be done for someone at risk of developing Retinopathy?

A

Fundoscopy - examining the fundi for hypertensive retina

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79
Q

What test should be done for someone at risk of developing CKD?

A
  • Urine sample to test for presence of proteins, using estimation of the albumin:creatinine ratio
  • Reagent strip for haematuria (blood in urine)
  • Blood sample to measure plasma glucose, electrolytes, creatinine, eGFR
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80
Q

What test should be done for someone at risk of developing an aortic aneurysm?

A
  • CT Scan
  • MRI Scan
  • Ultrasound
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81
Q

What test should be done for someone at risk of developing congestive heart failure?

A
  • Blood sample to measure serum total cholesterol and HDL cholesterol
  • May not be able to test, have to look at lifestyle and history
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82
Q

Describe the Renin-Angiotensin-Aldosterone System

A
  • Low BP
  • Sympathetic nerves switched on
  • Renin released from kidneys
  • Renin converts angiotensin to angiotensin I (this is inactive)
  • ACE enzyme converts angiotensin I into angiotensin II (active)
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83
Q

What does angiotensin II do?

A

Raises BP

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84
Q

How does angiotensin II raise BP?

A

*increase in Na+ and H2O retention:
-stimulate adrenal cortex to release aldosterone
-Na+ and H2O retained in kidney
-fluid volume increases
=increase in BP and Blood Volume (BV)
*Stimulate thirst
-increase fluid volume
=increase BP and BV
*Increase in water reabsorption in kidneys
-release of ADH form pituitary gland
-promotes water reabsorption in the kidneys
-fluid volume increases
=increase in BP and BV
*Causes vasoconstriction increasing blood pressure
*Cardiac and vascular hypertrophy
-more muscle mass
-increase in cardiac output
=increase in BP and BV

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85
Q

List some 5 lifestyle changes for someone with hypertension

A

Any 5 from

  • Improve diet
  • Decrease the salt in your diet. Aim to limit sodium to less than 2,300 milligrams (mg) a day or less.
  • Maintain a healthy weight, BMI
  • Increase physical activity. Regular physical activity can help lower your blood pressure, manage stress, reduce your risk of several health problems and keep your weight under control.
  • Limit alcohol.
  • Stop smoking.
  • Manage stress.
  • Control blood pressure during pregnancy.
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86
Q

Why might treatment for hypertension fail?

A

Lifestyle problems – weight, alcohol, exercise
Treatment ineffective – lack of compliance
White coat hypertension (patient has high levels of anxiety in hospital which results in hypertension)
Use of other drugs – sympathomimetics increase BP, amphetamine type drugs
Volume overload – Na intake, renal problems?
Unsuspected secondary cause – renal disease, endocrine disease

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87
Q

What symptoms would someone with atherosclerosis present?

A
  • weakness
  • facial or lower limb numbness
  • confusion
  • difficulty understanding speech
  • visual problems
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88
Q

What is Monckeberg’s arteriosclerosis/medial calcific sclerosis?

A

Mostly in the elderly, commonly in arteries of the extremities:
calcium deposits form in the middle layer of the walls of medium-sized vessels, and these vessels become calcified independently of atherosclerosis.

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89
Q

What is Hyperplastic arteriosclerosis?

A

Affects large and medium-sized arteries

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90
Q

What is Hyaline arteriosclerosis?

A

Deposition of homogenous hyaline in the small arteries and arterioles

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91
Q

What is a true aneurysm?

A

A localised permanent dilatation of the artery

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92
Q

What is a false aneurysm?

A

A blood-filled space around a blood vessel which does not penetrate the full wall thickness, may be limited to outer adventitia.

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93
Q

What is a dissecting aneurysm?

A

An intimal tear develops which allows blood to track into the media/muscle wall. Blood spreads along the media/muscle within the vessel wall forming a dissection. The patient may present with severe pain usually in the back, and often hypovolemic shock. As it spreads along, branches of the aorta are blocked, causing acute ischaemic damage.

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94
Q

What is the danger of having an aneurysm?

A

They can rupture, resulting in massive blood loss and likely death.

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95
Q

Posture has no effect on BP. True/False? Explain why

A

False
When lying flat, the pressure is all the same.
However, if you stand up quickly, fluid in the body drops down because of gravity. BP above the heart drops, whereas below the heart BP increases.

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96
Q

What is orthostatic hypertension?

A

When you stand up too quickly and your HR increases

Decrease in Systolic BP of greater than 20 mmHg after 2 minutes of standing compared to BP when lying flat

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97
Q

Describe the steps from standing up too quickly to baroreceptors being activated

A
  • Stand up too quickly
  • Drop in central venous pool (-500ml)
  • Venous return drops
  • Decrease in SV (-40%)
  • Decrease in CO (-25%)
  • Less O2
  • Increase in HR (+25%)
  • Total Peripheral Resistance (+25%)
  • Decrease in MAP
  • Baroreceptors activates
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98
Q

What are baroreceptors?

A

Mechanoreceptors located in the carotid sinus and in the aortic arch. Their function is to sense pressure changes by responding to change in the tension of the arterial wall. The baroreflex mechanism is a fast response to changes in blood pressure.

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99
Q

Describe the baroreceptor reflex when BP is low

A

-Decrease in MAP (decrease in baroreceptors firing)
-BP drops, baroreceptors are less stretched
-Signal sent to brain (specifically, medullary cardiovascular control centres)
-Brain sends signal to switch off Parasympathetic nerves
-Increase in SA node firing and Sympathetic nerves switched on
-Increase in HR and blood vessel constriction
This all feedbacks to baroreceptors

100
Q

Why does baroreceptor failure happen, an dhow can we treat it?

A

not enough blood in circulation to restore BP (diuretic, dehydrated, haemorrhage, damage to arteriole wall)
Can treat with anti-diuretic, drug that switches on alpha receptors - usually in elder patients

101
Q

What causes orthostatic hypertension?

A
  • hypovolaemia – use of diuretics, dehydration
  • vasodilators
  • prolonged bed rest
  • anaemia
  • Addison’s disease
  • atherosclerosis
  • diabetes and some neurological disorders
102
Q

How can we treat orthostatic hypertension?

A

Anti-diuretics, alpha 1 adrenergic receptor agonists (Midodrine)

103
Q

During exercise, CO output increases x5. Explain how this occurs.

A

*Increased myocardial activity
-Increase in venous return = more ventricular stretch
-Release of EP and NEP = Increased contractility
*Increased HR
-Vagal withdrawal (vagal tone - effect produced on the heart when only the parasympathetic nerve fibres, which are carried in the vagus nerve, are controlling the heart rate)
-Sympathetic nerves switch on
-Proprioceptors (receptors stimulated by movement) also prepare body for exercise.
*Atrial Booster Pump
-Venous return increase
-Skeletal muscle contracts
-Atrial wall stretched (more venous return = more stretch)
-More forceful contraction
(Compensatory for shorter diastole in exercise)
*Increased ventricular suction in diastole
-More blood pumped out
-Negative pressure in LV
-Blood ‘sucked’ from LA to LV

104
Q

CO increases during exercise. Describe the specific changes that happens to HR and SV.

A

HR x3

SV x1.5

105
Q

If a HR is 60bpm, what is the length of one cardiac cycle?

A

1 second

106
Q

If a HR is 180 BPM, what is the length of one cardiac cycle?

A

0.33 seconds

107
Q

If a cardiac cycle is 1 second, how long is Systole and Diastole within that?

A

Diastole - 0.67

Systole - 0.33

108
Q

What happens to diastole and systole during exercise?

A

The diastole:systole changes changes, but the length of the diastole is the limiting factor.

109
Q

What happens to SV when the HR is 200bmp?

A

SV decreases because there is not enough time for the ventricles to fill up (need at least 12 seconds)

110
Q

Venous return increases during exercise. How?

A
  • Skeletal muscle pump
  • Skeletal muscle contractions increase
  • Blood squeezes in veins = increase in venous return
  • Increased rate and depth of ventilation
  • Deeper breaths
  • Increase thoracic and abdominal negative pressure
  • Venous blood drawn into thoracic cavity = increase
  • Vasoconstriction of small veins
  • Sympathetic nerves cause small veins to vasoconstriction = increase in venous return
111
Q

What are the effects of exercising over time?

A

*Improved circulation
*Cardiac muscle increases (not pathological hypertrophy)
*Skeletal muscle increases
-develop more capillaries
-increase surface area
-reduce diffusion distance
-increase O2 deliverance
*Lower BP
*Cardiac physiological changes
-EDV increases
-SV increases
-lower resting HR
-Change in sympathetic and parasympathetic cardiac effect
=max HR doesn’t change much
*Improved endothelial function
*Improved lipid metabolism
-increase HDL
-decrease LDL
-reduced atherosceloritic changes

112
Q

Describe how waste is disposed in a clinical environment

A

Needles and sharp objects in ‘sharps’ bin
General waste in black bin
Soft clinical waste contaminated with infectious or potential infectious blood or bodily fluids in yellow/orange bin.

113
Q

Describe the steps in measuring BP

A

-Intro and explain
-Ask for full name and DOB
-Ask if BP taken before and have preferred arm
-Wash hands
-Cuff around arm at heart level
-Make sure arm is supported
-Fell the radial pulse for rate and rhythm
-Measure radial while inflating the cuff, stop when you can’t feel it anymore
-Fully deflate duff
-Record when pulse return = systolic estimate
-Palpitate brachial artery
-Re inflate cuff 20mmHg above systolic estimate
-Place stethoscope on brachial
-Deflate slowly at 2mmHg
-Listen for Korotkoff sounds (phase 1 is a thud and systole, phase 5 is the diastolic pressure).
-Documentation: time, date, name, grade, which arm, lying/sitting/standing and Systolic/Diastolic
-Thank patient and wash hands
Pulse pressure = Systolic Pressure - Diastolic Pressure

114
Q

How do you calculate mean BP?

A

Diastolic BP + 1/3 Pulse Pressure

115
Q

What are health and safety issuing surrounding venepuncture?

A

-Sharp needle; handle carefully and place in sharps bin when finished. Do not open until ready to be used, do not reinsert needles and do not re -use needles.
If needle stick injury: Encourage bleeding
Wash with soap and water
Attend occupational health 9-5 Mon-Fri
Attend A&E otherwise
Complete Datix form
*variable by trust
-Blood spills; clean up wearing gloves, inform colleagues and use specific cleaning products to clean blood
-Remember to remove tourniquet before taking needle out
-Wash hands before using needle
-Dispose of waste properly
-Wear gloves during blood taking

116
Q

What are some of the difficulties in recording BP?

A

-Korotkoff 1 and 3 sound similar
Estimation prevents this mix up in hypertension
-Diastole is actually at start of 4th sound, this is less reproducible
-Difficult to measure in hyper-dynamic states:
Pregnancy, hyperthyroidism, etc where 4th sounds never disappear

117
Q

Why might a radial pulse be regularly irregular?

A
  • Sinus arrhythmia (heartbeat too fast/slow)
  • 2nd degree heart block (electrical signals don’t pass from top to bottom of heart)
  • Bigemi (long, short, long heartbeats)
118
Q

Why might a radial pulse be irregularly irregular?

A
  • Ectoptic beats (premature heartbeats)

- Atrial fibrillation (fast)

119
Q

What does a collapsing/water hammer radial pulse suggest?

A

Aortic regurgitation (valve is leaking)

120
Q

What does a slow rising radial pulse suggest?

A

Aortic stenosis/anacrotic

121
Q

What is radial-radial delay?

A

When both radial pulses do not match in rhythm (or radial-femoral delay)
This is a sign of aortic coarction (congenital defect where aorta is narrow)

122
Q

What might a weak brachial pulse indicate?

A

Peripheral shutdown from hypovolaemia or heart failure

123
Q

What might a strong brachial pulse indicate?

A

Hyperdynamic state, could be from just exercising, pregnant or hyperthyroidism.

124
Q

What is a biphasic pulse?

A

In brachial, a double pulse. A sign of aortic stenosis or regurgitation.

125
Q

What is pulse coupling?

A

Heartbeat occurring in pairs

Sign of HOCM (Hypertrophic Obstructive Cardiomyopathy) or from digitalis toxicity (taking too much drug).

126
Q

What does a strong, weak, strong, weak brachial pulse mean?

A

LV systolic dysfunction

127
Q

What does brachial pulse that is weak during inspiration mean?

A 
SVC is obstructed
Constrictive pericarditis
Pericardial effusion (fluid building up in pericardium)
128
Q

What are bruits and what do they mean?

A

Murmurs in the carotid pulse, could be a sign of turbulent blood flow.

129
Q

What is the danger of having an embolism in the carotid artery?

A

Embolism is blocking of artery

Blocks blood supply to brain, leading to stroke

130
Q

What do you look for when checking pulses?

A

Volume, character, rhythm, rate

131
Q

Which pulses are affected by peripheral vascular disease?

A

Popliteal, posterior tibial, dorsalis pedis

132
Q

Name all the pulses checked in a pulse exam

A 
Radial
Brachial
Femoral
Carotid
Popliteal
Posterior tibial
Dorsalis pedis
133
Q

What does a narrow pulse pressure indicate?

A

Aortic stenosis, sclerosis, hypovolaemia

134
Q

What does a wide pulse pressure indicate?

A

Aortic regurgitation, stress, calcification in arteries

135
Q

What are disorders regarding HR?

A

Hypotension (from dehydration, sepsis, haemorrhage) or heart failure
Hypertension (from stress, renal failure)

136
Q

Describe all the phases of the Korotkoff sounds

A 
1 - Thud (110-120 mmHg)
2 - Blowing noise (100-110 mmHg)
3 - Softer thud (90-100mmHg)
4 - Disappearing blowing noise (80-90mmHg)
5 - Nothing
137
Q

What equation is used to calculate CO?

A

CO = HR x SV

138
Q

What is the equation used to calculate MAP?

A

MAP = CO x Total Peripheral Resistance

139
Q

What do baroreceptors do when BP is too high?

A
  • MAP is too high, baroreceptors are being stretched
  • Signal sent to brain (Medullary Cardiovascular control centre)
  • Brain sends signal to switch sympathetic nerves off and Parasympathetic nerves on
  • Parasympathetic neurons synapse on the SA and AV nodes. SA node effects reduce heart rate and thus cardiac output may reduce.
140
Q

How do Sympathetic nerves increase BP?

A
  • Sympathetic neurons synapse on the SA node (increasing heart rate) and on ventricular muscle (increasing force of contraction), thus cardiac output increases.
  • Sympathetic neurons also synapse on arterioles causing peripheral vasoconstriction which would increase TPR and thus increase blood pressure.
  • Sympathetic neurons also cause venoconstriction shunting venous blood into the arteries
141
Q

What is the BP in the arteries during diastole (ventricular relaxation)?

A

80mmHg

142
Q

What is the pressure range from diastole to systole?

A

4-5mmHg during diastole to 120 mmHg in systole

143
Q

How is BP maintained during systole?

A

The thick walled arteries maintain the pressure

144
Q

Why is diastolic pressure higher in the aorta than the LV?

A

Diastolic pressure stays higher in the aorta than in the left ventricle due to elastic recoil returning energy/pressure to the blood and closure of the aortic valve.

145
Q

Why does blood lose pressure as it travels along the vascular system?

A

As blood flows along the vascular system energy (pressure) is lost to the vessel walls due to friction thus reducing blood pressure. By the time the blood reaches the wide diameter, thin walled veins pressure has dropped to 4-5 mmHg.

146
Q

What factors determine MAP?

A
  • CO
  • Blood volume
  • Resistance of system to blood flow (peripheral resistance)
  • Distribution of blood between arterial and venous systems
147
Q

What determines blood volume?

A

Balance between fluid intake and fluid loss (which is regulated at the kidneys, or could be passive).
This doesn’t usually vary

148
Q

What determines CO?

A

HR and SV

149
Q

What determines Peripheral Resistance?

A

Diameter of arterioles - can modify MAP by changing this

More fluid in a fixed area also increases the pressure on the walls

150
Q

What determines distribution of blood between arterial and venous systems?

A

Diameter of veins

151
Q

What happens to the firing of action potentials from baroreceptors during hypotension?

A

Frequency decreases until it reaches 40mmHg, when action potentials stop.

152
Q

What can override the normal responses to maintaining MAP?

A

Sight of blood, fear, pain
Response: Intense increase in Cholinergic / sympathetic vasodilator supply to skeletal muscle arterioles = decrease in TPR
Intense increase in output from Inhibitory Cardiovascular Control Centre = decrease in HR
Overall, combined effect causes a rapid decrease in BP and reduced flow to brain
lose consciousness (faint)
Known as Vasovagal Syncope

153
Q

Describe the baroreceptor response when BP is too high

A

-Increase in MAP
-Baroreceptors sense this, are being stretched too much, increased frequency of action potentials firing
-Sensory neurones send message to cardiovascular control centre in brain = signals sent to Sympathetic and Parasympathetic nervous systems.
-Sympathetic – release less NE =
1.Arteriolar smooth muscle vasodilates = decrease in peripheral resistance
2.Sympathetic beta1 adrenergic receptor of Ventricular myocardium decreases force of contraction = decrease in CO
3.Sympathetic beta1 adrenergic receptor of SA node decreases in firing = decrease in HR = decrease in CO
All lead to BP decreasing
(All this is vice versa when BP is too low)

154
Q

Why can CCB’s cause oedema?

A
  • Decrease in arteriolar resistance
  • Disproportionate change in resistance increases hydrostatic pressures in the precapillary circulation
  • Fluid shifts into the interstitial compartment
155
Q

Where is K+ sourced from?

A

Major source of K+ is diet
Normal intake ~ 100mmoles K+/day
Source: meat, fruit and fruit juice

156
Q

Describe the distribution of K+

A

Plasma K+ concentration 4.5mmoles/l
Majority of K+ in intracellular compartment intracellular K+ concentration 140 mmoles/l
Intracellular compartment contains 40 000 mmoles ECF compartment 50 mmoles
Output: sweat 2mmoles/day faeces 8mmoles/day kidney ~90mmoles/day

157
Q

How does the body react to a meal with K+?

A

K+ intake in food is 100mmoles/day = exceeds total ECF pool
K+ needs to be buffered to stop rapid rise in plasma K+
Buffering is mediated by rapid uptake of absorbed K+ by RBCs, hepatocytes and muscle
• This is stimulated by aldosterone and insulin
• Over time kidney eliminates K+ and as plasma K+ falls then K+ is released from the RBCs, hepatocytes and muscle, over period of a day all K+ from meals eliminated

158
Q

What is hyperkalaemia?

A

High levels of K+ (plasma > 5.1mmol)

159
Q

What is hypokalaemia?

A

Low levels of K+ (plasma < 3.6mmol)

160
Q

What causes hyperkalaemia?

A
  • Increased dietary intake
  • Metabolic Acidosis
  • Hypoaldosteronism
  • Rapid shift of K from cells
  • -crush injury
  • Impaired renal function
161
Q

What are the effects of hyperkalaemia?

A
  • Excitable cells depolarise
  • Cardiac Arrhythmia - Increased risk of cardiac arrest
  • Abnormal neuronal conduction
162
Q

What causes hypokalaemia?

A
  • Loss of K - vomit diarrhoea
  • Metabolic Alkalosis
  • Diruetics - loop diuretics
  • Hyperaldosteronism
163
Q

What is in the retroperitoneal space?

A 
Suprarenal (adrenal) glands
Aorta / IVC
Duodenum (second and third part)
Pancreas (except tail)
Ureters
Colon (ascending and descending)
Kidneys
(O)Esophagus
Rectum (partly in pelvic)
164
Q

What is the retroperitoneal space?

A

Area of posterior abdominal wall that contains no viscera – this is an area where pus and blood can stay confined, or haemorrhages and infection may develop.

165
Q

What are the muscles of the abdominal wall?

Label on diagram

A
  • Psoas major (flexes hips) with iliacus, fuses together = main hip flexer. Comes from back of abdominal wall. Covered by faschia, inserts with muscle below groin area into femoral triangle. Infection in region can spread through faschia into femoral triangle. Blood vessels here, will be infected.
  • Psoas minor (not everyone has)
  • Iliacus
  • Quadratus lumborum
  • Transversus abdominis
  • Iliacus
  • Latissimus dorsi (back muscles)
166
Q

What are the muscles/ligaments of the abdominal wall?

Label on diagram

A
  • Psoas major (flexes hips) with iliacus, fuses together = main hip flexer. Comes from back of abdominal wall. Covered by faschia, inserts with muscle below groin area into femoral triangle. Infection in region can spread through faschia into femoral triangle. Blood vessels here, will be infected.
  • Psoas minor (not everyone has)
  • Iliacus
  • Quadratus lumborum
  • Transversus abdominis
  • Iliacus
  • Latissimus dorsi (back muscles)
167
Q

Name the branches of the abdominal aorta

A
  • Coeliac trunk comes off at T12 (foregut) supplies structures in digestive
  • Superior mesenteric artery (SMA) L1 (midgut)
  • Inferior mesenteric artery (IMA) L3 (hindgut)
168
Q

What supplies blood to the abdominal wall?

A 
Suprarenal arteries
Renal arteries come off aorta (L2
Testicular/ovarian (gonadal) arteries (L2)
Lumbar arteries
Median sacral artery
Abdominal aorta
Coeliac trunk (T12)
SMA (L1)
IMA (L3)
169
Q

Name the nerves of the abdominal wall

A

Nerves occur lateral (most) or medial (obturator) to psoas major muscle, or pierce through it (genitofemoral nerve)

Iliohypogastric Ilioinguinal (L1)
Genitofemoral (L1, L2)
Lateral cutaneous nerve of thigh (L2-L3)
Femoral (L2-L4)
Obturator (L2-L4)
Subcostal (T-12)
170
Q

What are the three capsules of the kidney?

A

Fascial (renal fascia)
Fatty (perinephritic fat)
True (fibrous capsule which strips readily from healthy kidney surface but firmly adherent when inflamed

171
Q

What are the segments of the kidney? (Label on diagram)

A 
Apical (A/P)
Anterosuperior (A)
Anteroinferior (A)
Posterior (A)
Inferior (A/P)
172
Q

What supplies blood to the kidney?

A

Highly vascular structure, complex circulation
Renal artery directly from aorta
Renal vein drains directly into IVC
Left renal vein passes in front of aorta immediately below the origin of the SMA
Right renal artery passes behind the IVC

173
Q

Describe the venous drainage system (label)

A 
Azygos, single system, single vein
Hemiazygos
Left renal
Lumbar
IVC, major system of drainage
Common iliac
174
Q

What openings are there in the diaphragm?

A 
Caval opening (T8)
IVC 
Right phrenic nerve coming out of IVC, none on left, phrenic nerve through thoracic into abdominal region. If phrenic nerve endings irritated by bleeding, signal travels up. Instead of pain in diaphragm, pain sensed in shoulder tip.

Oesophageal hiatus (T10)
Oesophagus emerges
Vagal trunks
Oesophageal blood vessels

Aortic hiatus (T12)
Aorta
Thoracic duct
Azygos vein

175
Q

Skeletal muscle in diaphragm moves involuntarily. True/False?

A

False

Does move involuntarily, but also moves voluntarily

176
Q

What makes the skeletal muscle in the diaphragm good for respiration?

A
  • Increased fatigue-resistant fibres for endurance
  • Higher oxidative capacity and larger blood-flow than limb muscles
  • 60% slow-twitch, good for endurance fibres
177
Q

Name the nerves which innervate the diaphragm

A
  • Mostly by phrenic nerve
  • C3, C4, C5
  • Marginal part is innervated by spinal nerves T6-12
  • Crura innervated by spinal nerves from T12
  • Diaphragm contracts as a single unit
  • Right phrenic nerve passes through caval opening (T8)
  • Left phrenic nerve passes through diaphragm itself
178
Q

What is the diaphragm?

A 
Dome shaped skeletal muscle
Superiorly:
Central tendon
No bony attachment fibrous pericardium is attached
Inferiorly: -attached to wall
Costal margin 
Posterior abdominal wall
Lumbar vertebrae
179
Q

Describe fascia in the kidneys

A

Kidneys lie in abundant fatty cushions (perinephritic fat), within renal fascia
Renal fascia above blends with fascia on undersurface of diaphragm  separate compartment for suprarenal gland
Fascia blends medially with sheaths of aorta and IVC
Fascia blends laterally with transversalis fascia
Only relatively open in inferior direction, tracking around the ureter into the pelvis

180
Q

Why are kidney stones dangerous?

A

Can get stuck in ureter and trap urine

181
Q

What stimulates ADH release?

A
  • High temp
  • Exercise
  • Pain
  • Heightened emotion
  • Stress
182
Q

Where is ADH made?

A

Posterior pituitry or supraoptic and paraventricular neurones
Stored in vesicles

183
Q

Describe how ADH responds (Osmolar)

A
  • Osmoreceptors (3rd ventricle) detect osmolality of cerebral fluid
  • if >280 Osm, ADH released
  • As osmolality increases, ADH increases
184
Q

Describe how ADH responds (Non-osmolar)

A
  • Decrease in blood volume by 10%

- ADH acts as vasoconstrictor (ADH is above amount needed to stimulate renal fluid absorption)

185
Q

How do baroreceptors stimulate ADH release?

A

Baroreceptors signs paraventricular neurones stimulation = release ADHA

186
Q

What is an osmostat?

A

In pregnancy, can reset to lower osmolality

187
Q

What are disorder in ADH secretion?

A
  • Hyponatremia (Na conc is < 135mM)

- Hypernatremia (Na conc is > 145mM)

188
Q

How does hyponatremia happen?

A

Gain in fluid and decrease in osmolality

189
Q

Describe how salt disturbances lead to hyponatremia

A 
Hypoaldosteroneism:
-lack of aldosterone
-less Na reabsorption in CD (Collecting Duct)
-loss of Na
Thiazide diuretics:
-inhibit coupled NacL cotransporters
-decrease in Na reabsorption
-Na lost in urine
-decrease in osmolality
-decrease in ADH secretion
-water lost and decrease in ECF volume
BUT 
-aldosterone released 
-increase Na reabsorption
-ECF volume back to normal
190
Q

Describe how disturbances of water intake lead to hyponatermia

A
  • Excess water intake (rare, usually kidney can handle it)
  • pscychological polydipsia (water intake increased because of metal illness)
  • Acute hyponatremia: in babies where formula is diluted too much (see in poverty)
  • Tap water instead of diaralyte after diarrhoea and vomit
  • innapropriate use of hypotonic IV solutions
  • use of ecstasy (induces extreme thirst)
191
Q

Describe how disturbances in water output lead to hyponatremia

A

Main cause is because of SIADH (Syndrome Inappropriate ADH Secretion)
ADH made when it’s not supposed to, keep more H2O than necessary
=less loss of water
-Also caused by CKD
-Too much water drank (overwhelms capacity to lose water = brain cells swell = coma = death).

192
Q

What causes SIADH?

A

-Lung disease
-Pain
-TB, pneumonia
-Brain/Spinal cord injury
-Can be drug induced
-Ectopic production from tumours (hormone released which interferes with metabolic functions)
-MDMA/Ecstasy
Increase in ADH and thirst reflex, decrease in Na conc and cerebral oedema. More water in than out
-Infection/fluid build up

193
Q

What is Hypernatremia?

A

Loss in fluid and gain in osmolality

194
Q

Describe how disturbances in salt balance lead to Hypernatremia

A

-Hypertonic saline/sodium bicarbonate/salt/mineralcorticoids in excess
= net gain of NaCl from body

195
Q

Describe how no ADH secretion leads to Hypernatremia

A 
Happens in Diabetes Insipidus (urine has high osmolality)
Central DI:
Injury (head trauma, hypoxia, ischaemia)
-damage to hypothalamus or osmoreceptors
-impaired secretion of ADH from pituitary gland (Treat with nasal spray of ADH - not net increase of osmolality of urine)
Nephrogenic DI:
-AVPR2 and AQP2 mutations
-V2 receptor and aquaporin defects
-Wash out medullary hypertonicity
-Can't have urine concentration
196
Q

Describe how disturbances in water intake lead to Hypernatremia

A

Lack of access to water because:

  • unconcious patient
  • caregiver gives fluid
  • lack of thirst response
  • refusal to drink
197
Q

Describe how disturbances in water output lead to Hypernatremia

A

Loss of ECF volume because:

  • Osmotic diuresis in Diabetes M
  • In burns patients
  • Excess sweating
  • Vomit and diarrhoea = loss of NaCl > loss of water
198
Q

What causes impaired renal response to ADH?

A

-Diabetes Insipidus
-Drugs
-Structural changes to kidney (urinary tract obstruction, sickle cell nephropathy, papillary necrosis)
Treat with ADH nasal spray

199
Q

Where is K+ handles in the kidney?

A
  • Proximal tubule
  • Loops of Henle
  • Distal tubule and collecting duct Principle cells
  • Collecting duct alpha intercalated cells
200
Q

What happens in the Proximal tubule in K+ regulation?

A
  • Reabsorption is mostly passive
  • Mainly restricted to late proximal tubule ( S2 and S3 segments)
  • Driven by the positive tubule electrical potential
  • And by paracellular solvent drag along with water
  • Accounts for around 70% of K+ reabsorption
  • Remains fairly constant % of filtered load and independent of dietary intake
201
Q

What happens in the Loops of Henle in K+ regulation?

A
  • Reabsorption mainly via Na-K-2Cl cotransporters
  • Small component of passive absorption driven by lumen positive electrical potential
  • Accounts for around 20% of K+ absorption
  • Remains fairly constant % of filtered load and independent of dietary intake
202
Q

What happens in the Distal tubule and collecting duct Principle cells in K+ regulation?

A
  • These cells mediate K+ secretion
  • Basolateral NaK-ATPase mediates K+ uptake into cells
  • Apical K+ channels mediate exit of K+ into lumen
  • Driving force is size of K+ gradient between intracellular [K+] and lumen [K+]
  • K+ secretion is between 0 and 180% of filtered load
203
Q

What happens in the Collecting duct alpha intercalated cells in K+ regulation?

A
  • These cells mediate K+ absorption
  • Apical K/H exchanger absorbs K+ from lumen
  • Driving force is H+ gradient
  • Can absorb up to 10% of filtered load
204
Q

Describe the steps in handling K+ in the kidney

A

(Late proximal tubule):
-Lumen is positive (lots of K+)
-K+ enters cells (Passive Paracellular Driven by potential difference)
Thick ascending loop of Henle:
-20% of K+ reabsorption from potential difference driving force
-Loop diuretic sensitive
Na-K-2Cl cotransporter – reabsorbs K+
Principle cells in collecting duct:
-Sodium channels in membrane reabsorb sodium
-Lumen now negative

205
Q

Describe the steps in handling K+ in the kidney

A

(Late proximal tubule):
-Lumen is positive (lots of K+)
-K+ enters cells (Passive Paracellular Driven by potential difference)
Thick ascending loop of Henle:
-20% of K+ reabsorption from potential difference driving force
-Loop diuretic sensitive
Na-K-2Cl cotransporter – reabsorbs K+
Principle cells in collecting duct:
-Sodium channels in membrane reabsorb sodium
-Lumen now negative (K+ can be excreted)
α – intercalated cells collecting Duct:
-Reabsorb potassium in exchange for proton
-High potassium in plasma = principle cell dominates (low K+, alpha cells dominate)
*Hormones control secretion and absorption

206
Q

What threshold has to be passed for K+ to be excreted?

A

Plasma concentration of K+ must be over 4.5mmol, the more K+ in cell, the more can leave
K+ leaves through concentration gradient

207
Q

Which hormone controls K+ reabsorption?

A

Aldosterone

208
Q

How is Aldosterone produced?

A
  • Increase in K+
  • Depolarisation of zona glomerulosa
  • Direct stimulation of aldosterone release into plasma
209
Q

How does Aldosterone control K+ reabsorption?

A

-Inserts more Na channels into apical membrane
-Inserts more Na/K ATPase into basolateral membrane
-Increased Na reabsorption generates larger lumen –ve (electrochemical gradient for K+)
potential difference which drives increased K+ secretion
-Provide more k+ into cell
Overall = Stimulates sodium reabsorption and potassium secretion

210
Q

Describe the relationship between urine flow rate and K+ secretion

A

Increase in urine flow rate = Increase in K+ secretion
K+ is in the lumen, which is close to the Principle cells, so this lowers the gradient. having a fast urine rate washes away the K+ from the lumen and increases the gradient = more K+ secretion

211
Q

How does acidosis lead to hyperkalaemia?

A

Increase in H+
To lower, plasma H+, protons taken into cell
in exchange for K+
- result is HYPERKALEMIA

212
Q

How does alkalosis lead to hypokalaemia?

A

Need to raise plasma H+
H+ exits cell in exchange for K+
- result is HYPOKALEMIA

213
Q

How does Hyperkalaemia lead to acidosis?

A

Need to lower plasma K+
K+ taken into cell in exchange for H+
- result is ACIDOSIS

214
Q

How does Hypokalaemia lead to alkalosis?

A

Need to raise plasma K+
K+ exits cell in exchange for H+
- result is ALKALOSIS

215
Q

Which cells act as buffers for K+?

A

RBC
Hepatocytes
Muscle cells

216
Q

What is the uptake of K+ stimulated by?

A

Insulin
Adrenalin
Aldosterone

217
Q

What causes CKD?

A
  • Glomerular disease (from immune disease or drug induced injury)
  • Vascular disease (Hypertension, Ischaemia)
  • Diabetes mellitus (Glomerular damage, Hypertension) Most common
  • Tubulointerstitial Disease, tubules are damaged, due to repeated infection. Scar tissue forms, can be from drugs or immune disease (Drug induced injury, repeated infection, immune disease)
218
Q

Describe the underlying pathophysiology of CKD

A

Progressive Destruction of Glomeruli (fragile structure)

219
Q

What are the clinical consequences of CKD?

A

-Blood disorder:
-Anaemia (not enough red cells)
Clotting Disorders (not enough white cells)
Bone disorders:
-Osteoporosis (bone thinning)
Neuromuscular disorders:
-Neuropathy (damage to nerves)
Skin disorders:
-Puritis & Itch (uncomfortable)
Gastrointestinal disorders:
-Anorexia
-nausea

220
Q

What is the treatment for CKD?

A

Difficult to reverse, can only relieve of symptoms.

Only way to treat if through kidney transplant

221
Q

Why does CKD cause anaemia?

A

-Kidney destroyed
-Less cells to make erythropoietin
-Bone marrow not stimulated to make RBCs
= feel weak, lethargic, rundown
Prone to more infections

222
Q

Why can CKD lead to Osteodystrophy (development of osteoporosis)?

A

Decrease in renal mass – less kidney working
Lots of phosphate in blood, not getting rid
of it
Phosphate conc in blood rises = parathyroid hormone released
Decreases phosphate being reabsorbed (renal problems stops this)
GI uptake of calcium drops
Loss of mass – increased parathyroid levels
Release of calcium from bone
Calcium levels increase, crystals of calcium phosphate precipitate out.
Cause itching in skin, they are forming in skin
All because phosphate can’t be removed

223
Q

Describe each stage of CKD

A

Stage 1 - Normal GFR, > 90 mL/min. Microalbuminuria present
Stage 2 - Mild CKDGFR, 60-89 mL/min. Parathyroid hormone starts to increase
Stage 3 - Moderate CKD.
Stage 3a GFR 45-59 mL/min
Stage 3b GFR 30-44 mL/min
Calcium absorption decreases
Malnutrition onset
Anaemia secondary to Erythropoietin deficiency
Left Ventricular Hypertrophy
Stage 4 - Severe CKD GFR 15-29 mL/min. Serum Triglycerides increase
Hyperphosphatemia
Metabolic Acidosis
Hyperkalemia
Stage 5 - End Stage CKD GFR <15 mL/min. Azotemia (uremia)

224
Q

When does CKD stop being asymptomatic?

A

Stage 4

225
Q

How does Ca being released from bones increase BP?

A

-Calcium reacts with phosphate groups
=Calcium phosphate deposited in tissues (endothelial cells of blood vessels_
-Calcification of arteries = rigid
-High BP = damage to blood vessels = heart disease

226
Q

What is pulmonary oedema?

A

Fluid build up in lungs (left side)

227
Q

What is peripheral oedema?

A

Fluid build up in lower limbs (Peripheral vascular system)

228
Q

Why do patients with CKD suffer from oedema?

A

-Kidney is damaged
-Limited ability to get rid of fluid
-Kidney gets wrong signals, blood flow is reduced
-Reduced perfusion of tissues
-Release of Renin
-Angiotensin II released = Vasoconstriction + Na uptake
AND
-Aldosterone released = Na reabsorption
=Hypertension and oedema (peripheral/pulmonery)

229
Q

Why is pulmonary oedema dangerous?

A

Fluid builds up in lungs, unable to transfer oxygen properly. Can lead to hypertension.

230
Q

Why do patients become dehydrated in CKD?

A

-Ischaemic damage to medulla
-Difficult to conserve water
-Loss of ability to make concentrated urine
=Risk of dehydration

231
Q

Why is Proteinuria dangerous?

A

-Proteins leak out, e.g. albumin (=microalbuminuria)
-COP (Oncotic pressure) decreases
-Fluid is leaving from blood, blood volume and pressure goes down
=balance of fluid entering and leaving blood disrupted
-interstitium get bigger = oedema

232
Q

How does Proteinuria happen?

A
  • In CKD, kidney is damaged
  • Glomerulus is damaged
  • Filtering is not as efficient, so proteins can leak out
233
Q

Why do patients with CKD develop Uremic Syndrome (Azotemia)?

A

-Kidney not functioning properly
-Nitrogenous metabolites (waste products)
not cleared from body
-Uremic toxins, kidney normally gets rid of these

234
Q

What is Uremic Syndrome (Azotemia)?

A

Excess of nitrogen compounds in the blood. Uremia, or uremic syndrome, occurs when the excess of nitrogen compounds becomes toxic to your system.

235
Q

Describe the pathophysiological consequences of Uremic Syndrome (Azotemia)

A

Blood: Platelet function and White cell function is disrupted
Neuromuscular system: Peripheral neuropathy
-Encephalopathy (affects brain and mental health)
-Motor neurone neuropathy
Gastrointestinal Tract: Nausea
-anorexia
-vomitting
-diarrhoea
-poor quality of life

236
Q

Why might patients with CKD show ECG abnormalities?

A

-Develop hyperkalaemia/excess K+ in blood

K+ involved in heart beating

237
Q

Why might patients with CKD develop Metabolic Acidosis?

A
  • Disturbances in acid-base balance
  • Unable to get rid of endogenous acid
  • Leads to Osteodystrophy (defective bone development)
238
Q

How is anaemia treated?

A

Erythropoietin

239
Q

How is Hyperphosphatemia treated?

A

Dietary restriction, GI phosphate binders, taken before meals - stops phosphate absorption

240
Q

How is Hypocalcemia treated?

A

Ca2+ supplements Calcitriol, stops hyperphosphatemia and osteoperosis, protect bones

241
Q

How is Fluid/ Electrolyte Imbalance treated?

A

Dietary modification, educate patients

242
Q

How is Uremia treated?

A

Dialysis, remove urinic toxins

243
Q

How is Proteinuria treated?

A

ACE inhibitors Diet, no real way of stopping.

244
Q

What is Haemodialysis?

A

Filtration of the blood through specialised dialysis membranes external to the body

245
Q

What is Ambulatory peritoneal dialysis?

A

Filtration achieved across the peritoneum. Fluid is instilled into the peritoneal space then drained.

246
Q

What is the issue with renal transplant?

A

Shortage of organ donors

Medicine (11 decks)

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