Week 9: Hypertension and Shock Flashcards

1
Q

Describe the hormonal counter mechanism for decreased blood flow to the kidneys

A
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2
Q

What are the 4 functions of angiotensin 2

A
  1. Angiotensin 2 actually also stimulates aldosterone to be released from the adrenal cortex
    - Aldosterone causes the reuptake of sodium (from the filtrate of the kidneys) within the kidneys
    - This causes the kidneys to retain water
    - Which increases blood volume, increasing arterial pressure
  2. At the same time, angiotensin 2 also stimulates ADH release from the posterior pituitary
    - ADH, or antidiuretic hormone increases aquaporins in the collecting duct
    - This increases the water reabsorption from the collecting duct back into the vascular
    - At high concentrations, this hormone also causes direct vasoconstriction, hence the name vaso – pressin
    - It also increases triggers the thirst mechanisms within the brain to increase blood volume
  3. It also has a direct vasoconstricting effect
  4. It works on the cardioaccelatory centre of the brain to increase cardiac output (same as baroreceptor reflex)
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3
Q

What stimulates the release of atrial natriuretic peptide?

A
  • Is the counter to the above-mentioned system, that deals with an increase in blood volume (which could overload the heart)
  • When there is elevated blood volume (and therefore blood pressure), the wall of the right atrium is stretched
  • The stretching causes stimulating of specialised cardiac muscle, that becomes secretory to release Atrial Natriuretic peptide (ANP)
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4
Q

What are the functions of Atrial natriuretic peptide

A

increased ANP causes the kidney to excrete more sodium and thus more water within the urine

  1. Hypothalamus
    - To reduce the secretion of vasopressin (ADH)
  2. Adrenal cortex
    - To reduce aldosterone secretion
  3. Medulla oblongata (cardio excitatory centre)

Decreased blood pressure

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5
Q

What are some reasons that would increase cardiac output and peripheral resistance (describe their flow chart mechanism), leading to an increase in mean artieral blood pressure

A
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6
Q

Fill the blanks

A
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7
Q

What harm does hypertension cause on the body?

A

· Increased afterload increases workload for heart -leads to heart failure, ischaemia, myocardial infarction

· Damage to major cerebral blood vessel followed by cerebral infarct (a stroke)

· Destruction of renal glomeruli, leading to renal failure

· Other target/end organ damge includes retinopathy and peripheral artery disease

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8
Q

What are the two types of hypertension

A
  1. Primary hypertension (also known as idiopathic or essential)
    - Idiopathic meaning we cannoty lock down an exact cause
    - We know it correlates with people who are obese, with high levels of plasma lipids, atherosclerosis, diabetes, stress (acute), drugs, high salt diet and a family history
    - However these are not a guarentee, some people can do all of the above and not have high blood pressure, it is simply a correlation
    - These are either described as constitutional (family history) or modiable/lifestyle risk factors (things we can control)
  2. Secondary hypertension
    - These are when the high blood pressure is secondary to another medical condition or medication
    - The cause and effect of this type of hypertension is ‘iron-clad’

Causes include; kidney disease, adrenal cortical disorders (release cortisol and aldosterone causing retention of sodium), pheochromocytoma (tumour that increases adrenaline), coarctation of the aorta, oral contraceptives (increase blood pressure), cocaine (acts as a stimulant of the SNS), erythropoietin (stimualtes RBC production) and licorice (prevents break down of cortisol in kidney

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9
Q

Why would renal artery stenosis (blockage in artery to kidney) increase the blood pressure in someone

What treatment could be used to solve this

A

one of the renal arteries are not producing blood flow to the kidney. Therefore, the kidney thinks there is decreased blood flow to one of the kidneys. It will therefore produce more renin.

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10
Q

What are some signs and symptoms of hypertension

A
  • Hypertension is typically asymtpomatic until it is very severe, at which point target organ damage has allready occurred (it is a silent killer)
  • Fatigue
  • Dizziness
  • Palpitations (dysrhythmias) (caused by the ischemia)
  • Angina (caused by ischemia)
  • Dyspnoea (reflects the high afterload causing pulmonary hypertension, then pulmonary oedema)
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11
Q

what are the constitutional risk factors that increase your risk for hypertension

A
  1. Age:
    - The older we are, the higher our blood pressure is
    - This is due to age related ‘wear and tear’
    - Atherosclerosis
    - Loss of arterial elasticity
    - This can be reversed through healthy diet, increased exercise etc.
  2. Race
    - Depending on what race you are you are going to have a higher or lower pre-disposition to hypertension
    - This genetic effect is independent of stress, age, diet etc.
  3. Gender
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12
Q

What are the 5 diseases that can be caused by chronic high blood pressure

A
  1. Hypertensive Heart Disease
    - Refers to the group of disorders that includes ischemaemic heart disease, left ventricular hypertrophy and heart failure
  2. Cerebrovascular Disease
    - Cerebral astherosclerosis causing ischemia to the brain, possible stroke, cerebral oedema
  3. Peripheral vascualr disease
    - Peripheral atheroscleoriss leads to periporeal vascular disease, aortic aneurysm and aortic dissection
  4. Nephrosclerosis
    - The increased blood supply should be combated by the affarent arteroiole myogenic vasoconstriction
    - However, after a while this value resets so that the high blood pressure is the normal value
    - This causes the pressure within the glomerular to increase, damaging and scarring the filtration system (reducing filtration)
    - This takes us towards renal failure (as glomerular cannot be replaced or fixed)
  5. Retinal Damage
    - Blurred and or loss of vision (caused by ischemia to the retinal blood supply)
    - Retinal haemorrhage (caused by increased pressure)
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13
Q

What are the lifestyle risk factors that increase risk for hypertension

A
  1. A high sodium intake
  2. Obesity
    - Bigger blood vessels, means longer blood vessesl, means increased friction and PVR
    - Also if they are obese they will have low physical fitness, or high lipid in the blood (not all obese people, but many due to a high lipid diet)
  3. Poor level of physical fitness
  4. Drug consumption
    - Excessive alcohol, caffeine and nicotine
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14
Q

What is the 1st methods of treatment you would treat someone with hypertension for?

A

1. Lifestyle modification

  • the first thing you do (as long as it is not severe) is try to modify the patients life style
  • if you can avoid giving your patient drugs that will cause problamatic side effects, that is the best course of action
  • if they are overweight encourage them to lose weight
  • if they eat a lot of salt or fat, encourage them to diet, encourage exercise, reduce alcohol consumption, convince to quit smoking
  • As shown by the below table, by inplementing these lifestyle changes patients can reduce their blood pressure significantly
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15
Q

There are two main avenues for shock. What is the 1st and the 3 under this subheading?

A

Diminished cardiac output

  • Cardiogenic shock: is caused by sytolic heart failure, which compromises heart contractility (can be caused also my MI)
  • Hypovolemic shock: Which is caused by reduced blood volume (from dehydration, haemorrhage)
  • Obstructive shock: Is caused by something that decreases venous return, restricting cardiac filling. Can also be caused by an obstruction of the outflow tract (e.g. pulmonary embolism)
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16
Q

There are two main avenues for shock. What is the 2nd and the 3 under this subheading?

A

Issues with distribution of blood to organs

  • Septic shock: when there is an bacterial infection, nitric oxide is produced which causes systemic vasodilation, meaning that the 5L of blood wont be enough to fill the vsaculature of the person
  • Anaphylactic shock: the inflamatory response assocaited with the allergy can also cause wide spread vasodilation and thus circulatroy shock
  • Neurogenic shock: Is caused by a spinal injury between the vagus nerve (PNS tone to the heart) and cardioacceleratory nerve (SNS tone to the heart) which cuts out the SNS input. This will cause a profound bradycardia within the heart. Severe vasodilation will occur
17
Q

What are the 3 compensatory mechanisms of circulatory shock

A
  1. Activation of baroreceptors
  2. Activation of chemoreceptors (at low blood pressure, blood flow is low enough that oxygen delivery is poor. This will lead to acidotic, hypercapnic with hypoxia which will trigger these chemoreceptor reflex affecting the SNS, cardioaccelatory centre, vasomotor centre to inhibit the cardioinhibitory system, aswell as influencing the respiratory rate)
  3. Activation of the RAAS
18
Q

What are the 3 stages of shock

A
  1. Non-progressive
  2. Progressive
  3. Irreversible
19
Q

What is non-progressive shock

A
  • This is known as compensated shock
  • The hypotension is not yet so overwhelming that it exceeds the capacity of the compensatory mechanisms to restore BP (everything can still do their job)
  • It makes patients uncomfortable, but is resolved within hours without intervention
  • Is associated with loss of 5 – 25% of the total blood volume
  • Pulse rate and respiration increases, there is a weak pulse, cool clammy skin, the patient will be anxious, thirsty and weak
20
Q

What is progressive shock

A
  • Is when the shock moves beyond a certain point, where the compensatory mechanisms are failing and cant maintian sufficient blood pressure to prevent cardiovascular deterioration and collapse
  • Characterised by a positive feed back loop, where the compensatory mechanisms are themselves compromised (they cant help as they don’t have enough oxygen themselves) making the shock worse spiralling down
  • The reduced perfusion starves the tissues of oxygen and nutrients causing deterioration of the patients condition
  • Known as decompensated shock, when the compensatory mechanisms are failing
  • You can pull patients back int othe compensated stage, however outside compensation has to be implemented
  • This occurs when 25 – 35% of blood volume is lost
21
Q

What are 5 characters of progressive shock

A
  1. Cardiac depression
    - Coronary blood flow is too low to provide adequate perfusion of the working heart muscle
    - Cardiac ischemia that stops the heart from doing its job
  2. Vasomotor failure
    - The smooth muscle of the Tunica Media is ischaemic which restricts its ability to maintian contraction (resulting in a loss of vasocontriction meaning it can no longer compensate for low blood pressure)
  3. Sludged blood
    - As blood is moving slowly, static blood tends to clot
    - Microvessels are blocked due to blood clots due to reduced blood flow
  4. Increase capillary permeability
    - Causing loss of plasma to the tissues, therefore reducing blood volume
  5. Release of toxins from ischemic tissues
    - Which results in vasodilation in an attempt to restore homeostasis decreases blood pressure
22
Q

What is irreversible shock

A
  • There is no coming back, that is no therapy (transfusion, drugs or antibiotics) can prevent death due to irreversible tissue damage
  • Even a blood transfusion is not enough as tissue damage is too great
23
Q

Describe the cascade that decreased cardiac output will result in

A
24
Q

What is the 2nd method of treatment you can treat someone with hypertension for?

A
  1. Pharmacological intervention
    - Move to this step if the lifestyle modifications arent working (or if the patient already has moderate to severe blood pressure)
    - The medications are effective, however can have annoying side affects
    - ACE-inhibitors, angiotensin 2 receptor blockers, aldosterone receptor blockers will all influence the renin-angiotensin-aldosterone system to reduce blood pressure
    - The most commonly prescribed are the ACE inhbitors, however due to their dry cough side affect (through the influence of bradykinin) put patients off the medication
    - Diuretics work nicely as they immediately decrease blood volume
    - Calcium channel antagonists preferentially target the L type voltage gated calcium channels in the vascular smooth muscle to decrease peripheral vascualar resistance to decrease blood pressure
    - Alpha adrenergic receptor blockers are also used as they cause vasoconstriction