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A Pathophysiology- BN607 > REVIEW LIST OF TEST 1- SPECIFIC! > Flashcards

REVIEW LIST OF TEST 1- SPECIFIC! Flashcards

1
Q

How does aging affect the cardiovascular system- THE HEART?

A

Myocardial ischemia progressively occurs, resulting in reduced myocytes and an increase in myocyte fibrosis.

Left ventricular hypetrophy typically occurs, as does valvular degeneration.Decreasing cardiac capacity and ability for the heart to cope with cardiac stress (e.g. exercise).

There is also a decrease in maximal heart rate (HR).

Reduced ability to increase cardiac output in response to increased tissue demands and an overall increased risk of heart failure.

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2
Q

How does aging affect the cardiovascular system- THE BLOOD VESSELS?

A

Decreased compliance of blood vessels. The aorta and larger arteries become stiffer due to decreased elasticity.

Generalized endothelial dysfunction with subsequent inflammation.Increase in atherosclerotic plaque formation within the vessels as a result of these changes.

Increase in blood pressure (systolic), though there is often a decrease in diastolic pressure.

Decreased ability for vessels to respond homeostatically to changes in blood pressure, meaning orthostatic hypotension becomes more common.

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3
Q

How does aging affect the cardiovascular system- HEMATOLOGY & IMMUNITY?

A

Decrease in erythropoiesis and lymphoid cell production. (erythropoiesis= RBC FORMATION). Thus overall decreases in cell counts and hemoglobin concentration.

There is decreased activity of the adaptive immune system due to decreased production of lymphocytes (B & T cells), but also due to decreased functionality of these cells, including memory cells.

There is a general increase in pro-inflammatory chemicals with an increase in inflammatory processes suspected to contribute to the aging process of many (if not all) tissues in the body.

Blunted fever response and WBC numbers do not increase as much in response to infection/trauma.Thus reduced wound healing and a decreased response to infection. Increasing infection susceptibility.

Increase in coagulability activity. Increases the risk of abnormal blood clot formation anddeep vein thrombosis.

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4
Q

How does aging affect the integumentary system- THE EPIDERMIS?

A

Decreased production and numbers of epidermal cells: keratinocytes, melanocytes and Langerhan’s cells.
- Reduction in cells causes the epidermis to thin, making it more permeable and losing its integrity.
Also causes increased water loss (drier skin) - wrinkles - and decreased immune barrier performance.

Decreased ability to make vitamin D – affects bones

The epidermal-dermal boundary also flattens with increasing age, further decreasing the integrity of skin.

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5
Q

How does aging affect the integumentary system- THE DERMIS?

A

 Epidermal-dermal Junction flattens – fragile; easy to shear skin
 May lose 20% of the dermal layer
 Decrease of collagen and elastin – causes wrinkles
 Capillaries become fragile – easy bruising
 Subcutaneous fat atrophies

Poor Temperature Regulation
 Decrease of hot and cold receptors of nervous system
 Decrease of subcutaneous fat, shivering, and loss of epidermis to protect from cold
 Decrease of sweat glands to protect from heat

Decreases in vascularity and nerve endings which contributeto decreased sensation and poor wound healing.

The subcutaneous layer also thins and atrophies due to decreases in adipocytes, which decreases heat conservation.

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6
Q

How does aging affect the integumentary system- ACCESSORY GLANDS?

A

Reduction in both sweat and sebaceous glands, with overall decreased secretion.Decreased sebum secretion further contributes to skin water loss and dryness.

Hair follicles reduce in number and hair thins, due to decreased keratinocytes,and colour fades within hair due to decreased melanocytes and melanin production within hair follicles.

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7
Q

What are the cardiovascular changes from aging that can increase blood pressure?

A

1) Decreased elasticity in larger arteries. (Become stiffer and less compliant.

2) Endothelial damage & inflammation

3) Atherosclerotic plaque formation

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8
Q

Describe at least two (2) changes that occur to the cardiovascular system with aging (11)

A

1) Progressive myocardial ischemia occurs
2) Myocyte reduction
3) Increase in myocyte fibrosis
4) Left ventricular hypertrophy occurs
5) Valvular degeneration
6) Reduced cardiac capacity- Especially with exercise
7) Decreased maximal HR
8) Aorta/large arteries loose in elasticity / become stiffer
9) Endothelial damage and inflammation occurs
10) Increase in systolic BP and decrease in diastolic BP
11) Decreased vascular response to changes in BP

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9
Q

How does a decrease in melanocytes affect the epidermis?

A

Decrease in melanocytes, so can’t repair the damage from UV light. UV light causes free radicals which cause mutations which cause cancer

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10
Q

What are dental carriers?

A

Demineralization of the teeth due to oral bacteria produces acid.

Acid production occurs when there are fermentable dietary sugars present and/or when there is decreased oxygen availability.

Most chronic disease in children- Incidence rate around 45%

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11
Q

What increases the likelihood of demineralization/ dental carriers

A
  • poor oral hygiene
  • minor tooth defects
  • decreased saliva function
  • inadequate fluoride
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12
Q

What are the stages of tooth decay/ dental carriers?

A
  1. Enamel lesions:
    demineralization of enamel resulting in chalky whitelesions (spots) on teeth
  2. Enamel decay:
    erosion (loss) of enamel resulting in yellow-brown discolouration
  3. Dentine decay:
    dentine breakdown as bacteria gain access to this part of the tooth resulting in cavitation
  4. Pulp involvement:
    decay reaches the pulp where bacterial infection can damage blood vessels and nerves
  5. Abscessformation:
    at base of root which increases likelihood of infection spread and damage to surrounding bone
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13
Q

What are treatments for dental carriers? (4)

A
  • plaque removal
  • removal of decayed enamel/dentine replaced with filling
  • root canal
  • removal of tooth/teeth
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14
Q

What prevents dental carriers?

A
  • good oral hygiene
  • limiting dietary sugars
  • application/administration offluoride
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15
Q

What is periodontal disease?

A

Periodontal (gum) disease is an inflammatory condition (induced by bacteria) affecting the periodontal tissues

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16
Q

What periodontal tissues does periodontal disease affect? (4)

A
  • gingivae (gums)
  • cementum
  • periodontal ligament
  • bone
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17
Q

What are the two kinds of periodontal disease?

A

Gingivitis & periodontitis

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18
Q

What is gingivitis?

A

Mild inflammation of the gingivae (gums) causing swelling, redness and likely bleeding (e.g. when cleaning teeth). If left untreated can develop into periodontitis.

Reversible with good hygiene

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19
Q

What is periodontitis?

A

Destructive gum disease associated with loss of gingiva surrounding tooth, leading to infection with subsequent further destruction of periodontal tissues and tooth loss.

Often associated with systemic inflammation.

Irreversible but has management options

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20
Q

What can periodontal disease develop? (4)

A
  • respiratory diseases
  • diabetes
  • skeletal conditions
  • preterm labour and low birth weight babies
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21
Q

What are management options for periodontitis? (4)

A
  • scaling
  • root planing
  • certain medications
  • surgery
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22
Q

What can poor oral health lead to? (5)

A
  • Dental caries
  • Preterm labour & birth
  • Tooth discoloration
  • Heart disease
  • Respiratory disease
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23
Q

What are the recommendations from the Ministry of Health for sustaining good oral hygiene/health? (6)

A
  • Brush your teeth twice a day.
  • Floss your teeth twice a day.
  • Reduce sugar
  • Stop smoking
  • Regular dental check ups
  • Use flouride
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24
Q

What is atherosclerosis?

A

Atherosclerosis thickening or hardening of the arteries

It is caused by a buildup of plaque in the inner lining of an artery.

Plaque is made up of deposits of fatty substances, cholesterol, cellular waste products, calcium, and fibrin.

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25
Q

What is coronary heart disease?

A

Coronary artery diseaseinvolves the narrowing, stiffeningand/or blockage of coronary arteries, mostly due toatherosclerosis.

This eventually causes myocardial ischemiawhich decreases functionality of the myocytes.

Due to the lack of available oxygen (O2), inflammatory chemicals are released and myocytes engage anaerobic respiration which can cause a build up of lactic acid.

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26
Q

What are risk factors to CAD?

A
  • Family history
  • Increasing age > 45 males, postmenopausal females
  • Hypercholesterolemia
  • Smoking
  • Hypertension
  • Diabetes
  • Obesity
  • Physical inactivity
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27
Q

What is angina?

A

Angina is chest pain that occurs when the oxygen demand of the myocardium outweighs the available supply. It is usually transient and typically occurs with increased physical exertion or stress.

Angina may be considered as:

  • Stable: angina is predictable (e.g. occurs with exertion) and resolves with rest or use of nitroglycerine
  • Unstable: angina is unpredictable, may occur at rest and is of increasing severity, length and/or frequency
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28
Q

What may be symptoms of angina?

A
  • pallor (an unhealthy pale appearance)
  • diaphoresis (sweating, especially to an unusual degree)
  • dyspnoea (Difficult or laboured breathing)
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29
Q

What is unstable angina typically associated with?

A

Unstable angina is often associated with atherosclerotic plaque rupture, or outer erosion which results in transient episodes of thrombotic occlusion and vasoconstriction.

Unstable angina is a strong predictor of myocardial infarction.

Management of unstable angina generally requires some type of antithrombotic (decrease coagulation factors)

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30
Q

What is a myocardial infarction?

A

Myocardial infarction occurs when there is sustained myocardial ischemia.

This usually occurs when an atherosclerotic plaque ruptures and a thrombus forms at the site causing coronary occlusion, but can also occur more rarely due to coronary spasm or dissection or other factors which can lead to significant ischemia/hypoxia (e.g. hypotension, anemia).

Prolonged myocardial ischemia leads to irreversible hypoxic damage.

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31
Q

What is heart failure?

A

Heart failure, sometimes known as congestive heart failure, occurs when there is inadequate perfusion (delivery of blood) of tissues due to cardiac dysfunction.

Heart muscle can’t pump enough blood to meet the body’s demands.

There is systolic HF and diastolic HF- Both causes blood back up in lungs- Congestion/ fluid buildup.

Multiple disease that can cause HF. EG- Valvular disease

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32
Q

What can HF be caused from?

A
  • MI
  • Cardiac hypertrophy
  • Chronic hypertension
  • Systemic or Pulmonary
  • Heart valve stenosis / incompetence
  • Cardiomyopathy e.g. viral, alcoholic
  • Volume overload in some patients
  • e.g. renal failure
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33
Q

What is systolic HF?

A

Systolic failure
* Heart failure with reduced ejection fraction (HFrEF)

The left ventricle loses its ability to contract normally. The heart can’t pump with enough force to push enough blood into circulation

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34
Q

What is diastolic HF?

A

Heart failure with preserved ejection function (HFpEF).

The left ventricle loses its ability to relax normally because the muscle has become stiff.

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35
Q

What is left sided HF and how does it develop?

A

Mostly systolic but can be diastolic.

The left ventricle of the heart no longer pumps enough blood around the body.

1) Blood build up in the pulmonary veins/ lungs ->
2) Pulmonary & venous BP increases to get blood out ->
3) pressure causes blood to leak into interstitial spaces of the lungs and alveoli ->
4) Pulmonary edema ->
5) Difficulty with gas exchange
6) Dyspnea, orthopnea (laying flat), crackle apon auscultation

Lung compliance is reduced - they become more difficult to inflate

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36
Q

What are symptoms of left sided HF?

A

Blood back up in lungs → increased pulmonary bp →
Fluid in interstitial space → pulmonary edema → difficulty gas exchange → dyspnea, orthopnea (laying tatt, crackles heard auscultation

  • Dyspnoea on exertion and fatigue
  • Cyanosis may reflect hypoxia

This causes shortness of breath, trouble breathing or coughing – especially during physical activity.

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37
Q

What is the most common cause of LHR?

A

Coronary artery disease- ischemia damages the myocardium

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38
Q

What is arteriosclerosis?

A

Arteriosclerosis is the thickening and hardening of the walls of arteries.

This occurs due to the migration of smooth muscle cells and collagen fibres into the tunica intima with subsequent mineral deposition.

Progressively this narrowsthe lumen of the artery.

Changes in lipid, cholesterol and phospholipid metabolism contribute to these changes in the blood vessel wall.

Arteriosclerosis occurs as part of the normal aging process, but may also occur in association with hypertension, decreased tissue perfusion, weakening and/or other damage of arterial walls.

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39
Q

What is Atherosclerosis?

A

Atherosclerosis is the most common type of arteriosclerosis.

When intra-arterial fat and fibrin deposits form within the vessel wall which subsequently harden over time.

Atherosclerotic plaques can form as a result of inflammation due to endothelial damage and the accumulation of LDL cholesterol within the tunica intima.

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40
Q

What are the risk factors of atherosclerosis?

A
  • family history
  • increasing age (>45 males, postmenopausal females)
  • hypercholesterolaemia (increased LDL)
  • smoking
  • hypertension
  • diabetes
  • obesity
  • physical inactivity
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41
Q

What is PAD?

A

Peripheral artery disease is a type ofperipheral vascular disease (PVD)caused by atherosclerosis within arteries.

Mostly found within the lower limbs

It is commonly associated withdiabetes and coronary artery disease and has the same risk factors as atherosclerosis.

Arterial atherosclerotic obstruction in PAD can be gradual or acute. It can be asymptomatic, or may present with symptoms

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42
Q
A
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43
Q

What are symptoms of PAD?

A
  • intermittent claudication: pain/cramping in the lower limbs when moving/exercising
  • changes in skin of lower limb (e.g. temperature, colour, appearance)
  • leg ulcers
  • weak or undetectable pulse in legs or feet
  • severe pain with acute occlusion
  • gangrene
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44
Q

What are some treatment options for PAD?

A

Anything that can reduce associated risk factors (e.g. smoking cessation, increased exercise)

Management/treatment options used for any associated conditions (e.g. diabetes).

Additionaltreatment options may include
anti-platelet therapy, anti-coagulation therapy, vasodilators andif required, vascular surgery or angioplasty.

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45
Q

What is a deep vein thrombosis?

A

Thrombosis is a pathological formation of a blood clot (thrombus) within an intact vessel.

This can occur in either arteries or veins, but is more common in veins.

The thrombus partially (or completely) occludes the lumen of the vessels-

in arteries this can cause tissue ischemia/infarction and in veins can cause localized inflammation.

Deep vein thrombosis is when thrombosis occurs in the deep veins of the limbs, generally the lower limbs.

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46
Q

What are risk factors of DVT formation

A
  • surgery
  • immobilization
  • obesity
  • dehydration
  • smoking
  • pregnancy
  • coagulopathies (a condition in which the blood’s ability to coagulate (form clots) is impaired)
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47
Q

What are symptoms of a DVT and how are they resolved?

A

Many DVTs are asymptomatic, but they may also present with
Tenderness, pain in leg, increased warmth, red/blue leg, discomfort when pulled upward and/or oedema of the affected limb.

Many DVTs will resolve on their own due to the breakdown of the clot, however, some DVTs may become organized and remain within the vessel- potentially becoming incorporated into the vessel wall and/or recanalising.

DVTs also carry the risk of becoming dislodged and forming anembolus.

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48
Q

What can prevent DVT?

A
  • mobilizing as soon as possible after periods of immobilization (e.g. due to injury or surgery)
  • maintaining adequate hydration
  • avoiding standing or sitting or long periods of time
  • using compression stockings when mobility will be reduced for a period of time

While most DVTs will resolve on their own, if DVT is suspected it is common for anticoagulants to be used to facilitate resolution of the clot.

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49
Q

What is virchow’s triad - factors that contribute to thrombosis

A

Endothelium damage
Altered blood flow
Hypercoagulability

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50
Q

What is asthma?

A

Asthma is a chronic inflammatory condition that results in narrowing of the airways in response to various triggers (e.g. allergens).

It is not known what causes asthma, but it is likely that both genetic and environmental factors play a role.

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51
Q

What is the pathway of air inhalation?

A

Trachea - Bronchi - bronchioles - alveoli - capillaries surround alveoli

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52
Q

What are some asthma attack triggers?

A

Pollen, smoke, pollution, cold weather, mold pet dander, dust mites, fish, eggs, peanuts, soy

Respiratory conditions, stress, strong emotions and exercise.

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53
Q

What are some symptoms to an asthma attack?

A

Coughing, wheezing, SOB, chest tightness.

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54
Q

What is an asthma attack also known as

A

Bronchospasm

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55
Q

What is the physiology of an asthma attack?

A

Smooth muscles tighten, the endothelium bronchiole lining inflames and excess mucus production + oedema

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56
Q

What can can asthma attack cause?

A

The increased airway resistance reduces both air flow into and out of the lungs. Thus, there is a V/Q mismatch which leads to hypoxemia (Reduce blood oxygen), and subsequently hypoxia if not relieved.

Air retention and hypercapnia (to much co2 in blood) also occur. If airflow is significantly limited, an asthma attack can be life threatening.

There is no cure for asthma, but treatment options can be used both preventatively and responsively.

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57
Q

What is cystic fibrosis?

A

An autosomal recessive condition which results in abnormalities of secretory epithelia throughout the body (e.g. respiratory tract, pancreas, GI tract).

Though significant morbidity is associated with the effects on the respiratory system.

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58
Q

Why does CF cause thicken mucus?

A

In CF there are certain mutations that cause the CFTR ion channel is either not there or made incorrectly, meaning chloride ions cannot exit the cell.

Broken CFTR increases activity of a different ion channel called the ENaC channel. ENaC allows sodium ions to enter the cell (leaving mucus). Due to the ion gradient osmosis occurs - water leaving the mucus

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59
Q

What are the effects of CF on the lungs

A

In the resp system the mucus so abnormally thick and sticky that the cilla cannot move it through the escalator. Leading to infection & death. Mucus can clog airways making breathing difficult.

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60
Q

What are the effects of CF on the GI tract?

A

Gall bladder ducts that transport bile & enzymes from the pancreas into the small intestine can lead to mucus build up in the ducts.

Malnutrition occurs as the food cant get digested properly.

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61
Q

What are the effects of CF on the sweat glands?

A

OPPOSITE OF AIRWAY AND GUT- Channels normally allow chloride ions to enter the cell.

In CF chloride cannot enter the cell and accumulates outside the body. Chloride combines with sodium ions and forms salt.

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62
Q

What are the main symptoms of people living with CF?

A

Difficulty breathing from clogged airways and infected airways.
Malnutrition from clogged and defective ducts
Salty sweat

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63
Q

What are the most common ethnicities to have CF?

A

In order- Caucasians, African Americans & Asians

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64
Q

What are some medications for CF?

A

Digestive enzymes and vitamin supplements.
Antibiotics
Mucolytics (They break up mucus)
Bronchodilators

ONLY HELP SYMPTOMS

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65
Q

What can chronic infections and inflammation do to the respiratory system?

A
  • abscess & cyst formation
  • bronchiectasis (Permanent dilation of bronchi, typically as a result of inflammatory damage to bronchial walls due to previous chronic infections.)
  • pneumonia (fluid or pus)
  • pulmonary hypertension & cor pulmonale
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66
Q

What are some treatment options for CF?

A

chest physiotherapy
positive pressure devices
inhaled mucus thinning solutions
antibiotics
nutritional supplementation & enzymes

67
Q

What is Gastroesophageal reflux disease (GORD/GERD)?

A

This is a chronic condition where by reflux occurs frequently. The acidic stomach contents irritate and damage the mucosal lining of the oesophagus and this can lead to persistent oesophagitis (Oesophagus inflammation)

Due to incompetent sphincters at the gastroesophageal junction

68
Q

What is peptic ulcer disease?

A

Peptic ulcers are breaks (ulceration) in the mucosa of the stomach or duodenum.

This break in the surface mucosa exposes the deeper layers of the GI tract wall to gastric acid and digestive enzymes which can then erode away those deeper layers.

69
Q

What are the two kinds of peptic ulcers and what is the most common?

A

Gastric ulcers and duodenal ulcers

Most common is the duodenal ulcers.

70
Q

What is the stomach mucosa made from?

A

Mucus and bicarbonate to neutralize the acid

71
Q

What breaks down the mucosa/protective stomach layer?

A

Medications (steroids or NSAIDS), helicobacter pylori 7 increase of acid

72
Q

What causes an increase of acid production in the stomach?

A

Stress, alcohol, excessive caffeine, smoking, spicy food

73
Q

What are symptoms of peptic ulcers?

A

Epigastric discomfort or pain or tenderness
Nausea or vomiting
Dyspepsia (Indigestion)
Haematemesis (vomiting blood)
Coffee ground blood (Vomiting digested blood)
Melaena (Tarry black stool from digested blood)
Iron deficiency anemia

74
Q

How can you differentiate between a gastric ulcer and a duodenal ulcer?

A

Eating worsens gastric ulcer
And eating improves the pain of duodenal ulcer

75
Q

How do you diagnosis a peptic ulcer?

A

Endoscopy- Can do a biopsy to exclude cancer and a rapid urease test to see if its H. pylori

76
Q

How do you manage a peptic ulcer?

A

High dose of protein pump inhibitor - reduce acid
Endoscopy- monitor ulcer & see if it heals or find more ulcers

77
Q

What are complications of peptic ulcers?

A

Low level bleeding- anemia
Life threatening- Hemorrhage

Perforation- Hole in stomach. Stomach fluid can leak out into the peritoneum- Peritonitis (inflammation) URGENT- Requires surgery

Scaring and strictures (an abnormal narrowing of a bodily passage). As ulcer heals, turns into scar tissue- Narrowing of the pylorus - difficulty emptying the stomach- Pyloric stenosis - Causes upper abdominal pain, nausea and vomiting, reflux, distention

78
Q

What is crohn’s disease

A

Inflammation of Crohn’s disease starts in the submucosal layer and spreads to affect all layers of the intestine (all layersof the GI tract wall).

Changes to the mucosa cause the gut to be more
permeable, which can allow in toxins

Exacerbations and remissions

There can be so much inflammation that the lumen
actually narrows and the gut may become obstructed.

Often requires surgery

Most commonly in the proximal colon and small intestine, but could occur anywhere along the GI tract. GUM TO BUM!

The repeated inflammation can lead to fissures,fistulas,adhesionsand damage to theentericnervous system. MINI ULCERS THAT CAN OCCUR ANYWHERE IS THE DIGESTIVE TRACT. Ulcers cn causes inflammation. Can break through the wall and cause abscess.

It can also result in malnutrition or nutritional deficiencies, as intestinal absorption is impacted.

79
Q

What is symptoms of crohns?

A

Skip lesions – lesions will form in select places, but other parts of the gut will be normal; lesions are more common on the right side

Symptoms: Diarrhoea. Because small intestine is involved, digestion and absorption are affected. May have very fatty diarrhoea. Blood can occur but is less common.

Complications: Fistulae, strictures. Anemia from being
unable to absorb vitamin B12

80
Q

Whats ulcerative colitis?

A

Inflammation breaks down the mucosal layer which can cause abscesses.

Ulcerative colitis only happens in the colon (large intestine). Inflammation of themucosa (ONLY MUCOSA)of the GI tract wall, most commonly in the distal colon (e.g. sigmoid colon).

Repeated inflammation can lead to the formation of haemorrhoids, anal fissures or abscesses. Hemorrahge is also a complication of ulcerative colitis.

81
Q

What are symptoms of UC?

A

Symptoms: Large, watery, often bloody diarrhoea with cramping(mild to severe)

Pattern of exacerbation and remission
Exacerbations can come with fever, tachycardia, 10-20
stools per day, continuous cramping

Complications can include anal fissures, haemorrhoids,
perirectal abscesses

Colon can be obstructed – but rare. Rare perforation

82
Q

What are symptoms of chrons and ulcerative colitis?

A

Stomach pain
Weight loss
Decreased appetite
Changes in bowel movements
Urgent movements
Fever
Night sweats
Tiredness
Mucus and blood in stool

83
Q

What medications are used to managed crohns and UC?

A

Corticosteroids, immunosuppressants & biologics (antibodies that inhibit molecules that cause gut wall inflammation)

84
Q

Define hypercapnia

A

Too much carbon dioxide in the blood

85
Q

Define hypoxemia

A

Not enough oxygen in the blood

86
Q

Define hypoxia

A

Not enough oxygen to the tissues/ cells

87
Q

Define Cor pulmonale

A

Right ventricular enlargement and failure

88
Q

Gastroesophageal reflux disease (GORD/GERD) is most commonly due to

A

Incompetent or compromised oesophageal sphincter

89
Q

What are the GI wall layers affected in UC?

A

Mucosa only

90
Q

What are the GI wall layers affected in crohns?

A

All layers (mucosa > submucosa > muscularis externa > serosa)

91
Q

What portion of GI tract most commonly affected by UC

A

Distal colon

92
Q

What portion of GI tract most commonly affected by crohn’s

A

Proximal colon & small intestine

93
Q

What is anemia?

A

Anemia is a reduction in the oxygen carrying capacity of red blood cells (decreased hemoglobin concentration and circulating RBCs).

This reduction may be due to:
- reduced numbers of RBCs (decreased production, increased destruction or increased loss)

  • reduced amount of hemoglobin in RBCs
  • defective RBC/hemoglobin structure or development

There are many different types of anemia. Terms ending with -cytic refer to the size of the RBC and terms ending with -chromic refer to the hemoglobin content of RBCs.

94
Q

What are common symptoms of anemia?

A
  • fatigue
  • feeling cold/cold peripheries
  • pallor
95
Q

What are additional signs and symptoms of anemia that are less common?

A
  • dizziness
  • shortness of breath
  • heart palpitations or signs of cardiac distress
  • gastrointestinal effects such as nausea, abdominal pain, anorexia
  • neurological effects such as numbness, muscle weakness, spasticity
  • epithelial changes such as hair/nail brittleness,koilonychia,glossitis,stomatitis,cheilosis
  • jaundice
96
Q

What is Iron deficiency anemia?

A

Iron deficiency anemia is the most common form of anemia worldwide.

Anemia due to iron deficiency.

In a single RBC there is thousands of haemoglobin proteins. Inside hemoglobin there are four heme molecules. In the heme molecules there is iron. Iron is what binds to the oxygen. So each heme molecule can bind to 4 oxygen molecules.

Can be caused from:
- inadequate dietary intake of iron
- inadequate absorptionof iron
- increased iron requirements
- excessive iron loss

97
Q

What does iron deficiency do to RBC’s?

A

Iron deficiency leads to impaired heme productions- Not enough heme to make a normal sized RBC- Bone marrow begins to make microcytic RBC that contain less hemoglobin-
Iron deficiency is also called microcytic hypochromic anemia.

These RBC cant carry enough oxygen to RBC- hypoxia

Bone marrow try to pump out more RBC, subsequently forming incomplete RBC with varying shapes and sizes

Also causes defective production of of mitochondrial enzymes.

98
Q

What are specific symptoms caused by iron deficiency anemia

A

Koilonychia (spooning of nails)
Hair loss
Pica (consumption of non food items like clay or dirt)
Glossitis (inflammation of the tongue)
Esophageal webs(are thin membranes that grow across the inside of the upper part of the esophagus and may cause difficulty swallowing)

99
Q

How can you diagnose iron deficiency anemia?

A

DECREASED
- Hemoglobin
Males- less than 13.5 g/dl
Females- less than 12.0 g/dl

  • Decrease in mean corpuscular volume (MCV)- Reflects the volume of a RBC
  • Low serum iron & ferritin

INCREASED
- Total iron binding capacity (TIBC)- Amount of unbound transferrin in the blood.
- High RBC distribution width (RBW)- Different RBC size

Peripheral blood smear can determine wheather a person has microcytic & hypochromic RBC

100
Q

What is treatment for iron deficiency anemia?

A
  • Addressing the cause
  • Giving oral iron supplements (Ferrous sulphate)
  • Intravenous Iron
  • Severe cases call for blood transfusion
101
Q

What is macrocytic anemia?

A

Macrocytic anemias are those in which the RBCs are too big, due to immaturity. Though the cells may be normochromic, the structural immaturities mean they do not have the same oxygen carrying capacity as normal RBCs (they also do not live as long).

This can happen due to folate (folic acid)or vitamin B12deficiency.

Folate and vitamin B12 are required for DNA production in the developing RBCs. Without them, there is incomplete development of the erythrocytes (they remain immature) andless of them are produced.

102
Q

How can folate deficiency anemia occur?

A
  • inadequate dietary consumption or absorption: linked to risks associated with poor diet or conditions affecting small intestinal absorption (e.g. Coeliac disease)
  • alcoholism: associated with vitamin malabsorption, decreased liver metabolism of folate & increased urinary output of folate
  • dialysis: increases renal loss of folate
  • certain medications
  • increased demand during pregnancy: folate is important for early neurological development of the baby (inadequate folate can lead toneural tube defects) and thus there is increased demand that may not be met by dietary intake and which may be impacted by changes in absorption of folate during pregnancy
103
Q

How can vitamin B12 deficiency occur?

A
  • inadequate dietary consumption: linked to risks associated with poor diet or conditions affecting small intestinal absorption. More rare than folate
  • certain medications
  • lack of intrinsic factor (pernicious anemia):
    1) chronic atrophic gastritis: results in destruction of parietal cells
    2) removal of all/part of stomach: decreases numbers of parietal cells
    3) autoimmune conditions which destroy parietal cells

Why does a lack of intrinsic factor (IF) lead to vitamin B12deficiency? Because IF is necessary for intestinal absorption of vit b12

104
Q

What are some other kinds of anemia?

A

Anemia of chronic disease (Anemia associated with chronic infections or inflammatory disorders (e.g. systemic lupiserythromatosis).

Hemolytic anemia
Post-hemmorhagic anemia
Aplastic anemia
Thalassemia
Sickle cell anemia

105
Q

What is polycythemia?

A

Polycythemia is excessive RBCs.

Polycythemia increases blood viscosity, thereby increasingblood pressure, and it also increases the risk for thromboembolism and associated complications.

Treatment typically includes removal of some blood (phlebotomy/venesection), to maintain safe levels of hematocrit, and treating any underlying causes or complications.

106
Q

What is relative polycythemia?

A

Relative polycythemia is increased RBCs associated with dehydration and is readily corrected with fluid administration

107
Q

What is absolute polycythemia?

A

Absolute polycythemia can occur as-

  • Primary polycythemia (polycythemia vera): excessive production of RBC believed to be associated with a gene mutation. This condition is very rare.
  • Secondary polycythemia: occurs due to increased erythropoietin (EPO) secretion. Increased EPO secretion may be associated with the presence of certain tumours oras a response to chronic hypoxia, as may occur with:
    • living at high altitude
    • COPD or coronary artery disease
    • smoking
108
Q

What is Disseminated intravascular coagulation (DIC)?

A

Disseminated intravascular coagulation (DIC) is a thrombohaemorrhagic disorder that involveswidespread thrombusformation throughout the microvasculature, followed by hemorrhage.

DIC is triggered by events that cause severe endothelial damage such as may occur with:

  • sepsis
  • malignancy
  • severe trauma
  • pregnancy/labour complications
  • hemorrhage
  • hypovolemic shock

When severe endothelial damage- excessive coagulation response- This drives widespread formation of many thrombi throughout the microvasculature- Subsequently, tissue ischemia occurs leading to hypoxic tissue damage- The damaged tissues respond by enhancing tissue factor & procoagulants, thus leading to more and more micro-thrombi formation throughout the vasculature.

The widespread formation of many thrombi also leads to an increase in fibrinolysis (It prevents blood clots) via plasmin activation. Thus, as widespread clot formation occurs, widespread clot breakdown also occurs.

Eventually, coagulation factors (clotting factors and platelets) are all used up and further blood clots cannot be formed. This, coupled with the ongoing fibrinolysis, leads to hemorrhage and eventually hypovolemic shock.

109
Q

What manifestations of Disseminated intravascular coagulation (DIC) mostly relate to hemorrhage

A
  • petechiae (pinpoint non-blanching spots), purpura (occurs when small blood vessels leak blood under the skin), ecchymoses (bruise)
  • bleeding from minor wounds, venepuncture sites
    bruising
  • bleeding from mucous membranes
  • signs related to internal tissue damage and hemorrhage (e.g. respiratory distress, convulsions, signs of shock or organ failure)
110
Q

What is Cancer?

A

Cancer is a group of diseases characterized by genetically altered cells.

This genetic alteration leads to uncontrolled and abnormal growth of these cells and the formation of tumours or neoplasms.

Tumours/neoplasms can form from any type of cell, but are not always cancerous.

111
Q

What are Benign tumors?

A

Benigntumours contain cells that appear normal. Noncancerous. The cell growth is typically self-limiting and the tumour is encapsulated. There is no spread to other tissues.

The abnormal cell growth and additional cells themselves may not be a problem, but the size or location of the tumour may impact on nearby structures, thereby potentially impacting on normal body functions.

112
Q

What are malignant tumors?

A

Malignanttumours are cancerous. They are distinguishable from benign tumours by:

  • rapid or unregulated growth: not affected by normal signals that regulate growth or destroy damaged tissue
  • lack of cellular differentiation (anaplasia)
  • absence of normal tissue organization

Malignant tumour growth occurs due to abnormalities and mutations in genes. The reasons for these genetic abnormalities are not always known, but there are many likely causes, including genetic predisposition and/or environmental factors.

113
Q

What does gene malignant tumours cause in regards to cell activity?

A

The gene alterations that occur in cancer cells are permanent and result in the following changes to cellular activity & control:

  • uncontrolled cell proliferation: cancer cells do not respond to normal signals to reduce or stop growth (e.g. from neighboring cells)
  • control of growth signals: cancer cells secrete their own growth signals (autocrine secretion) and/or upregulate growth factor receptors
  • disables cellular apoptosis mechanisms: cancer cells do not undergo normal self-destruction
  • restoration of telomeres: the normal cell aging and division process leads to progressive shortening of telomeres which ultimately results in cell damage and cell death, but as cancer cells restore telomeres, they can continue to divide indefinitely
114
Q

What are few genes that have been identified in cancer development?

A
  • proto-oncogenes
  • tumour-suppressor genes
  • DNA repair genes
115
Q

What is proto-oncogenes?

A

Proto-oncogenes: genes coding for proteins that regulate normal cell growth.

Genetic mutations in proto-oncogenes give rise tooncogenes. Oncogenesallow unregulated cell proliferation & differentiation. Oncogenes can be activated by minor alterations to the genes, resulting in altered protein activity. Oncogenes can also cause chromosome amplifications- multiple duplications of a chromosome segment, thereby increasing expression of the gene (e.g. for growth receptors).

116
Q

What are tumour suppressor genes?

A

Cancer inhibits the tumour suppressor genes:

Tumour suppressor genes coding for proteins that:
- slow or stop cell division
- initiate DNA repair
- enhance immune system detection &destruction of cancer cells
- trigger apoptosis

117
Q

What are DNA repair genes?

A

DNA repair genes: genes coding for proteins involved in repairing damaged DNA

DNA damage occurs daily in cells- in normal circumstances DNA repair genes are activated to repair the damage with no sustained effects.

If there is a defect, or mutation,in these genesand DNA repair cannot occur appropriately, this can give rise to cancerous development of cells. Different types of DNA repair genes have been implicated in different types of cancers.

118
Q

What are the risk factors for cancer?

A

Immunity, inflammation & infection, Chemical exposure, Radiation, Dietary factors

119
Q

What is Cancer staging?

A

Cancer staging outlines the tumour size and level of spread, with higher stages attributed to larger sized tumours and more spread. There are different cancer grading systems, but most systems account for:

  • tumour location, size and/or type
  • involvement of lymph nodes
  • involvement of other tissues (metastasis)
120
Q

What is stage 0? cancer

A

Abnormal cells are present but have not spread to nearby tissue. Also called carcinoma in situ, or CIS. CIS is not cancer, but it may become cancer.

121
Q

What is stage 1, 2 & 3? cancer

A

Cancer is present. The higher the number, the larger the cancer tumor and the more it has spread into nearby tissues.

122
Q

What is Stage IV (may also be written as Stage 4) cancer

A

The cancer has spread to distant parts of the body.

123
Q

Distinguish between tumour grading and cancer staging?

A

tumour grading compares the tumor cells to the host tissue cells and awards a grade based on the level of resemblance

Cancer staging is about the size tumour and level of spread. In both cases the higher the grade/stage the more severe the cancer is

124
Q

What do the letters TNM stand for in this cancer staging system?

A

T= Size and the extent of the tumour
N= Number of lymph nodes with cancer
M= Whether or not metastasis occurs

125
Q

What is Leukemia?

A

Leukaemia is cancer of blood-forming tissues, including bone marrow.

1) Blast immature cells accumulate in bone marrow
2) cells cant mature
3) cytopenia (Decrease cells: WBC, RBC & platelets)
4) Immature cells spill into blood and accumulate in other tissues.

It isrelated to excessive proliferation of particular hematopoietic cells which may remain undifferentiated or are not fully mature/functional. The cell type, and it’s stage of differentiation, determine the different types of leukemia which may be either acute or chronic

126
Q

What is acute leukemia?

A

Acute leukemia develops rapidly with the highly proliferative blast cells taking up space in the bone marrow and preventing the normal development of all types of blood cells, resulting incytopenia.Eventually the malignant blast cells spill out into circulation and may then spread to other organs and tissues in the body.

Acute: there is rapid proliferation of undifferentiatedblast cells(immature blood cells)

  • Acute lymphoblastic leukemia (ALL): lymphoid stem cell lineage
  • Acute myeloid leukemia (AML): myeloid stem cell lineage
127
Q

What is chronic leukemia?

A

Chronic: there is slower proliferation of more differentiated cells in the lineage, but the cells do not achieve full maturity

  • Chronic lymphocytic leukemia (CLL): lymphocyte cell lineage
  • Chronic myeloid leukemia (CML): myeloid cell lineage
128
Q

What increases the risk of leukemia?

A

Like other cancers, leukemia is associated with the development of abnormalities in the genes of the affected cells (e.g. chromosomal translocation). These genetic abnormalities may be inherited or acquired. Though the specific cause of the genetic damage may not be known, some of the following factors are believed to increase the risk:

  • other genetic/hereditary conditions (e.g. Downsyndrome)
  • exposure to certain toxins/chemicals, such asbenzene
  • chemotherapy or radiation therapy
  • other blood cancers or disorders
  • certain infections (e.g. HIV)
129
Q

What is lymphoma?

A

Lymphomas are neoplasms that develop from lymphocytes within the lymphatic system. There are two main types of lymphoma:

  • Non-Hodgkin’s lymphoma
  • Hodgkin’s lymphoma

In either case there are genetic abnormalities that develop within lymphocytes- B-cells (most commonly), T-cells or NK cells- that result in uncontrolled proliferation of malignant cells.The growing neoplasms disrupt the normal function of healthy WBCs within the lymphatic system, decreasing effectiveness of the immune & lymphatic systems in fighting infections.

130
Q

Signs & symptomsof lymphoma may include?

A
  • painlesslymphadenopathy (common sites: cervical, axillary & inguinal lymph nodes)
  • B symptoms. (Unexplained fever, drenching night sweats and weight loss)
  • fatigue
  • pruritis (Itchy skin is an irritating sensation that makes you want to scratch)
  • abdominal symptoms(associated with abdominal masses orhepatosplenomegaly)
  • mediastinal mass,cough or chest pain (associated with mediastinal node involvement)
131
Q

What is non-Hodgkinlymphoma?

A

Non-Hodgkinlymphoma more commonly occurs in middle age and the tumour cells readily spread to other lymphoid tissues and organs, which may be sporadic. Sub-types may be of the aggressive (fast-growing) or indolent (slow-growing) variety.

Risk factors**include:

  • family history
  • certain toxins/chemicals
  • irradiation
  • certain viral infections (e.g. Epstein-Barr, HIV)
  • Helicobacter pyloriinfection
132
Q

What is Hodgkin’slymphoma?

A

Hodgkin lymphoma is distinguished from Non-Hodgkin lymphoma by the presence of Reed-Sternberg (RS) cells. (Reed-Sternberg cells are large, abnormal lymphocytes (a type of white blood cell) that may contain more than one nucleus)

Spread also tends to occur in a more continuous pattern (e.g. from one group of lymph nodes to another). There are two major sub-types:
classical Hodgkin lymphoma and
nodular lymphocyte predominant Hodgkin lymphoma.

Lymphoma tends to affect young adults or more elderly adults.

Risk factorsinclude:
- previous infections with Epstein-Barr virus
- HIV infection

Treatmentoptions vary based on the specific type of lymphoma and the staging of the disease, but most treatment includes chemotherapy and/or radiation. Stem cell transplant might be an option in some cases and in other cases drug therapy may be beneficial.

133
Q

With lymphoma, malignancy of lymphocytes occurs within the…

A

Lymphatic system

134
Q

What are the stages of infection?

A

Incubation: pathogen is replicating, but no signs/symptoms have developed. Different pathogens have different incubation periods.

Prodrome: initiation of signs/symptoms (typically mild & vague) while pathogen continues to replicate.

Illness: period of significant signs/symptoms (typically more severe) specific to the infection.

Decline: decline in signs/symptoms as elimination of pathogen enhances.

Convalescence/Resolution: signs/symptoms disappear, infection has been contained/eliminated.

135
Q

What is HPV?

A

Human papillomavirus (HPV). Group of non enveloped DNA virus’s. Specifically infection human epithelia cells. Categorised by what epithelium it infects- Can affect cutaneous tissue or mucus membranes.

There are 200+ different varieties of HPV.

Can cause begine tumors, warts and carcinomas.

Transmission: skin-skin contact (particularly with broken skin), sexual contact (some varieties).

136
Q

What are symptoms of HPV?

A

Warts, precancerous lesions and carcinomas

137
Q

Which of the following sexually transmitted infections has a high association with cervical cancer?

A

HPV

138
Q

What HPV virus strains are responsible for the majority of laryngeal, papillomatosis and genital warts?

A

6 and 11. Classed as low risk HPVs and they dont ever really progress further than warts

139
Q

What HPV virus strains are classed as high risk and can develop into cancer

A

16 and 18

140
Q

What are respiratory treatments ?

A
  • High flow oxygen
  • Beta-agonist drugs: inhaled or intravenous
  • Anticholinergics (bronchodilators)
  • Corticosteroids
  • Adrenaline
  • CPAP (continuous positive airway pressure)
  • SaO2 & Cardiac monitoring
  • Severe forms may require sedation, intubation and mechanical ventilation
  • Antibiotics
  • Chemotherapeutics
141
Q

When should oxygen be prescribed?

A

Oxygen saturation levels below 92% in room air, and patients should be weaned from oxygen when the saturation level exceeds 94%

142
Q

What medications are given in the event of an asthma attack?

A

Sympathomimetics (bronchodilators) relax bronchial smooth muscle via stimulation of the enzyme adenylcyclase

Immediate relief medications include:
- Salbutamol (Brand name ventolin)
- Terbutaline
They are short acting and target beta 2 adrenergic receptors on bronchial smooth muscle

143
Q

What sympathomimetics are used in asthma mangement?

A

Sympathomimetics (bronchodilators) relax bronchial smooth muscle via stimulation of the enzyme adenylcyclase

Immediate relief medications include:
- Salbutamol (Brand name ventolin)
- Terbutaline

Long acting relief:
Salmeterol (Brand: servent) - Long acting inhaler, prevent inflammation, promotes bronchodilation

144
Q

What are side effects of sympathomimetics?

A

Tachycardia, palpitations, tremor and anxiety

145
Q

What Anticholinergic drugs are used for asthma?

A

Ipratropium (Brand: Atrovent)
Inhibits bronchoconstriction

146
Q

What corticosteroids are used for asthma?

A

Hydrocortisone- IV for asthma 100-200mg

Both glucocorticoid and mineralcorticoid properties

These types of drugs switch on/off specific genes that code for proteins involved in the inflammatory process or its regulation. They can take hours to exert the full therapeutic effect. USED ONLY IN SEVERE CASES

147
Q

What Methylxanthines are used for asthma?

A

Methylxanthines- (Intravenous Brand: Aminophylline) (Oral Brand: Theophylline) - Inhibits bronchoconstriction

148
Q

Whats CPAP?

A

CPAP

Applies continuous positive airway pressure to keep airways open throughout the breathing cycle

In spontaneously breathing patients low levels of mask CPAP may improve respiratory rate, dyspnoea, and work of breathing in asthma

There is a danger that CPAP may worsen lung hyperinflation

If patients are intolerant of the mask or do not benefit, CPAP should be withdrawn

In hypercapnic patients CPAP alone may not improve ventilation

149
Q

What are some cardiovascular drugs?

A

Diuretics
Sympathomimetics – α, β receptor drugs, nerve terminal drugs
α, β receptor drugs, nerve terminal drugs – calcium channel blockers
Antigiotensin antagonists - ACE inhibitors, receptor blockers
Anticoagulants
Statins

150
Q

What are sympathomimetics used for?

A

Used to increase cardiac contractility E.g digoxin
or
decrease contractility E.g. β2 agonists dilate skeletal and coronary arteries and therefore decrease “afterload” and myocardial workload

aswell used for CF

151
Q

What are some sympathomimetics? CARDIO

A

Beta blockers e.g. metoprolol, propranolol
Competitively block beta1 adrenergic receptors on the S.A. and A.V. nodes of the heart as well as on the ventricular muscle cells

Reduce heart rate and contractility therefore ↓cardiac output and blood pressure

Because the heart rate is reduced there is also more time for blood to move from the aorta to other areas of the circulation

Aortic blood pressure therefore reaches lower levels during diastole and so afterload is reduced

152
Q

What are advantages to Sympathomimetics- Beta blockers

A

Advantages of beta blockers

-The reduction in rate and force of contraction reduce cardiac output and BP

  • This →↓ myocardial workload and oxygen consumption
    This class of drugs may sometimes be used to treat angina and heart failure.
    Caution using these drugs in heart failure because while they may reduce myocardial workload if cardiac output declines it may make the situation worse
  • Proven over 30 years to reduce blood pressure and incidence of fatal and non-fatal stroke
    Also used in treatment of myocardial infarction and heart failure but less validated
153
Q

What are disadvantages to Sympathomimetics- Beta blockers

A

Disadvantages of beta blockers

  • Fatigue/depression
  • Vivid or bad dreams
  • Provocation of asthma
    also block β2 receptors on bronchiole smooth muscle ⇒bronchoconstriction
    metoprolol more selective for β1 receptors than earlier drugs such as propranolol
  • Cold peripheries
    blockade of β2 receptors that dilate some blood vessel
  • Possible conduction block or heart failure
  • May increase serum triglycerides
154
Q

What are some Vasodilators- calcium channel blockers

A

E.g. nifedipine, felodipine

Vascular smooth muscle cells have only small amounts of stored calcium ions, Calcium ions are necessary for muscle contraction because they permit the interaction of actin and myosin

Calcium ions enter through voltage gated calcium channels when the muscle cell is depolarised

Blocking these channels in vascular smooth muscle causes less calcium to be available intracellularly and so the force of contraction is reduced → vasodilation and reduced TPR

Unwanted effects ‐ excessive vasodilation, hypotension, dizziness, flushing, ankle oedema. Calcium channel blockers may also worsen heart block and heart failure

Verapamil is a calcium channel blocker that binds more to calcium channels on cardiac muscle and pacemaker cells so may be more useful in treating some arrhythmias e.g. SVT

155
Q

What are some Proton pump inhibitors?

A

Omeprazole, Pantoprazole and other “prazole” medications are drugs that affect out proton pump inhibitors in the stomach wall

They are the most potent inhibitors in the gastrointestinal tract

Omeprazole irreversibly inhibits the H+/K+-ATPase ie. proton pump which is the final step in the acid secretory pathway

They reduce the acid secretion by up to 99%

Omeprazole is a neutral pH but because it is a weak baseit accumulates in the canaliculi of parietal cells where it is activated and has specific action on these cells

Unwanted effects are uncommon but may include: headache, diarrhoea, rashes, dizziness, pain in muscles & joints

156
Q

What are infections penicillin can treat?

A

Clinical uses of penicillins
The first penicillins were the naturally occurring benzylpenicillins

Benzylpenicillin (penicillin G) remains a useful antibiotic, active against a wide range of bacteria (provided these organisms are beta-lactamase negative) including:

Streptococcal infections
Pneumococcal infections
Gonococcal infection
Meningococcal infection
Treponema (syphilis)
Clostridium (tetanus, gas gangrene)
Diptheria, anthrax, leptospirosis

157
Q

What are the Penicillin V & G medications

A

Phenoxymethylpenicillin (V)
- Similar antibacterial spectrum as benzylpenicillin but less active

  • Gastric acid stable
  • Not be given for serious infections because absorption is unpredictable
  • Mainly used for:
    respiratory tract infections in children
    streptococcal tonsillitis
    continued oral treatment

Benzylpenicillin (G)
- Inactivated by gastric acid

  • Best given by injection
  • Allergic reactions can cause convulsion at higher doses
  • Beta-lactamase positive
158
Q

What are some broad spectrum penicillins?

A

Aminopenicillins
Piperacillin & Ticeracillin
Flucloxacillin

159
Q

What is process of systolic LSHF?

A

unable to pump → myocardial damage → cant contract Forcefully → Pumps

160
Q

What is causes of systolic LSHF?

A

1) Most common: ischemia ( CAD) → Damage to myocardium.

2) long standing HTN: Increased in bp in systemic circ → hard to pump blood in high pressure system → muscle hypertrophy → Increased 02 demand, for the Increased in muscle → Increased muscle squeezes the CA → tissue ischima x hypoxia → weaker contraction

3) Dilated cardiomyopathy: LV dilated to fill more blood & increase contraction strength → work for a bit → muscle walls get to thin & weak → unable to pump

161
Q

What diastolic LSHF?

A

Cant relax during diastole

162
Q

What are the causes of diastolic LSHF?

A

1) long standing HTN → concentric hypertrophy → less filling room

2) Aortic stenosis (aortic valve narrows and blood cannot flow normally) → concentric hypertrophy

3) Hypertrophic cardiomyopathy (Build of muscle mass) → less filling room

4) restrictive cardiomyopathy → stifter & less compliant → cant stretch & fill

163
Q

What does a reduction in CO from heart failure cause?

A

reduation blood to kidneys → renin-Angiotenin Aldosterone system → fluid retention → increased filling reload → increased contraction strength →
Good for a while → blood retention in the blood vessels → leak into tissues → Fluid build up in lung & body

A Pathophysiology- BN607 (28 decks)

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