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Cardiorespiratory 2 PBL > PBL 1 > Flashcards

PBL 1 Flashcards

1
Q

define atrophic glossitis

A

glossitis is soreness and inflammation of the tongue, atrophic glossitis is when papillae on the tongue are worn away leaving the tongue glossy and red

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2
Q

define angular stomatitis

A

this is an inflammatory condition that affects the corners of the mouth

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3
Q

define intramuscular hydroxocobalamin

A

man made B12 that is injected into the muscle

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4
Q

define haemodialysis

A

– method of removing excess fluid and salt and wastes from the blood and thus replacing the excretion functions of the kidneys

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5
Q

define hypersegemented neutrophils

A

– this is the presence of hypersegemented neutrophils as. Diagnostic feature of megoblastic anaemia

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6
Q

Define anaemia

A

this is a condition in which there is a deficiency of red cells or of haemoglobin in the blood, the levels to define anaemia vary in men and women

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7
Q

what are the limits of anaemia for men and women

A

less that 12.2 for women
less than 13.7 for men
(measurements of haemoglobin per g/dl)

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8
Q

define haemoglobin

A

– this is a red protein that transports oxygen in the blood in red blood cells, it contains 4 proteins which contain an iron bound to a haem group

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9
Q

define reticulocytes

A

– these are immature red blood cells, they have a reticular appearance when stained with methylane blue stain

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10
Q

define erythropoietin

A

this is a hormone that is secreted by the kidneys in the interstitial cells of the proximal convoluted tubules and increases the rate of production of red blood cells in response to hypoxia

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11
Q

what is the EPO response to anaemia

A
  • These can be different depending if it is due to dimished oxygen carrying capacity in the blood such as haemoglobin or a decrease in the erythrocytes
  • If someone is anaemic then they could have a lack of oxygen that is circulating due to less haemoglobin if the red blood cells are microcytic, this would be noticed by the EPO in the interstitial cells of the proximal convoluted tubule and this would therefore cause an increase in the amount of red blood cells by acting on erythropoietic stem cells
  • EPO is in the proximal tubule as oxygen levels remain constant and do not change with blood pressure and exercise here
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12
Q

what is the CVS response to anaemia

A
  • There is also an increase in cardiac output, this is due to the amount of haematocrit decreasing therefore the afterload decreases so this increases stroke volume and thus cardiac output
  • There can also be redistribution of cardiac output, the blood flow is redistributed to the tissues such as the brain and heart
  • There is increased oxygen extraction, and a decrease in mixed venous oxygen saturation, less oxygen available therefore more oxygen is removed from the tissues
  • Oxyhaemoglobin dissociation curve shifts to the right, this is because haemoglobin as a decreased affinity for the oxygen molecule therefore releases oxygen to the tissues at higher partial pressures
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13
Q

what are the basic mechanisms that lead to anaemia

A
  • Impaired ability of the bone marrow to produce RBC
  • Destruction and loss of RBC
  • Lack of production of haemoglobin
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14
Q

describe the formation of red blood cells

A
  • It starts with a haemotopoietic stem cell or a haemocytoblast which differentiates into a stem cell called a common myeloid progenitor or proerythroblast (ready for growth to a erythrocyte)
  • The proerythroblast undergoes a series of transformations where its nucleus progressively shrinks (condenses) and its cytoplasm becomes filled with haemoglobin until it becomes a reticulocyte and is released into the blood.
  • Normoblast becomes a reticulocyte,
  • The proerythroblast develops into an erythroblast. The erythroblast then undergoes successive changes where its nucleus progressively shrinks and its cytoplasm becomes filled with haemoglobin.
  • Finally the nucleus is expelled and it becomes a reticulocyte most of which stay in the marrow to become erythrocytes but some may be released into the blood. Reticulocytes can mature into adult RBCs in the circulation
  • The final stage of development is when the mature reticulocyte expels the nucleus and the newly formed erythrocyte squeezes through pores in the marrow capillary membrane into the blood by a process known as diapedesis
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15
Q

describe the destruction of red blood cells

A
  • After ~120 days old (senescent) RBCs are removed from the blood by macrophages as they pass through the spleen.
  • One way the spleen detects old RBCs is by their lack of deformability. Old cells become more rigid and this enables them to become entrapped in the spleen capillaries.- monitored by the macrophages
  • Trapped RBCs are engulfed by splenic macrophages and broken open by osmotic lysis.
  • The haem (in USA: heme) prosthetic groups are removed from the globin proteins and the globin protines are broken down to amino acids
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16
Q

describe how the haem is broken down

A
  • The haem is then broken open by the haemoxygenase enzyme. Iron atoms from haem are collected by transferrin. Transferrin carries the iron in the blood to the liver and thence the bone marrow where it can be re-used to make new haemoglobin.
  • The opened porphyrin ring minus its iron atom is now called BILIVERDIN (so-called because it has a greenish colour
  • Biliverdin is then reduced to BILIRUBIN (which has a yellowish colour) in the macrophage by biliverdin reductase.
  • Bilirubin is more stable than biliverdin
17
Q

describe how bilirubin is broken down

A
  • Stuck to albumin in the spleen and then the albumin bilibrubin is released into the blood
  • Bilirubin is not very soluble. It binds to albumin in the splenic macrophages and the complex released into the blood. This is called unconjugated bilirubin.
  • When the unconjugated bilirubin reaches the liver it is attached to glucuronic acid by the hepatocytes to make it more soluble. When bound to glucuronic acid it is called conjugated bilirubin.
  • Normal level of conjugated bilirubin in the blood is 0.1-0.3 mg/dL
  • Conjugated bilirubin passes in the bile to the small intestine where bacteria convert it into urobilinogen.
  • Most urobilinogen passes out of the body in faeces but about 10% passes back in the portal vein to the liver. The recycled urobilinogen leaves the liver in venous blood. When it passes through the kidney it is excreted in urine (giving it its yellow colour
18
Q

what gives urine its yellow colour

A

urobilinogen

19
Q

describe the size of red blood cells and how they lead to anaemia

A
  • Red blood cell size can be used to classify anaemia
  • There is microcytic anaemia which is when the red blood cells are too small <80fl
  • There is macrocytic anaemia which is when the red blood cells are too large >96fl
  • There is normocytic anaemia which is when the red blood cells are normal size 80-96fl
20
Q

what things cause microcytic anaemia

A
  • Iron defiency
  • Anaemia of chronic disorders
  • Thalassaemias and haemoglobin E train
21
Q

what things cause macrocytic anaemia

A
  • Alcohol
  • Vitamin B12 or folate deficiency
  • Drug intake
  • Haemolysis
  • Liver disease
  • Thyroid disease
22
Q

what things cause normocytic anaemia

A
  • Acute blood loss
  • Anaemia of chronic disorders
  • Anaemia of renal failure
  • Haemolytic anaemia
  • Anaemia of endocrine disease
  • Early iron deficiency anaemia
  • Mixed iron and vitamin B12/folate deficiency
  • Sickle cell disease
23
Q

what are the symptoms of microcytic anaemia with lack of iron

A
  • Tiredness – lack of oxygen
  • Shortness of breath – lack of oxygen
  • Increased constipation
  • Blood in stools
  • Pale – less haemoglobin therefore less redness towards the skin
  • Atrophic glossitis – low levels of iron mean that there are low levels of myoglobin, this is a molecule that has an important role in all muscles in the body
  • Angular stomatitis/cheilitis – lack of iron
  • Low haemoglobin – hyperchromic – reduced haemoglobin production due to iron deficiency
  • Microcytic anaemia
  • Microcystic red blood cells
  • Normal white blood cells
  • Normal platelet count
  • Normal reticulocytes
24
Q

describe patient 1

  • explanation
  • causes
  • tests
A

Explanation
- Lack of iron means lack of haem groups therefore the oxygen cannot bind to the haemoglobin therefore there is reduced circulation of oxygen leading to tiredness and shortness of breath
Iron deficiency – due to low iron in diet, reduced red blood cell synthesis, excess iron loss may be due to bleeding – blood in stool inflammatory disorder, high stomach pH, hookworm, - need to test ferritin, take ferrous sulphate tablets, improve diet

Causes

  • Taking NSAIDS
  • Stomach ulcers
  • Swelling of the large intestines or food pipe
  • Piles
  • Cancers of the bowel or stomach but this is less common

Tests

  • Blood in stools mean there is bleeding in the digestive tract
  • Could be due to, piles, anal fissure, bowel cancer
25
Q

describe treatment for patient 1

A
  • Treatment of iron deficiency anaemia involves iron tablets that replace the iron that is missing in the body
  • Can eat more meat, cereals and bread with extra iron in them, dark green leafy vegetables
  • Eat less tea and coffee, milk and dairy and other things that can stop the body from absorbing iron
26
Q

describe patient 2 signs and symptoms

A
  • Pallor and difficulty walking – lack of oxygen
  • Shortness of breath – lack of oxygen
  • Tingling in her hands and feet (paraesthesia) – B12 deficiency
  • Unsteadiness – B12 deficiency
  • Pale – lack of haemoglobin
  • Mildly jaundice
  • 110 heart rate – slightly high – lack of B12
  • 135/85 – slightly high – lack of B12
  • Cant stand for more than a minute – Nervous system problem due to lack of B12
  • Really low haemoglobin
  • Macrocytic anaemia
  • Macrocytic red blood cells
  • Low white blood cell
  • Low platelet
  • Hypersegemented neutrophils – megaloblastic anaemia
27
Q

what is the explanation and cause for anaemia in patient 2

A

Explanation

  • Lack of B12 or folate, B12 in this case, causes the body to produce abnormally large red blood cells
  • Megaloblastic anaemia – due to nervous system issues, HSN, paraethesia, gait issues
  • Due to lack of B12 or folate, these vitamins serve as building blocks and are the precursors to the production of red blood cells as ell of DNA
  • PERNICIOUS ANAEMIA IS. ATYLE OF MEGALOBLASTIC ANAEMIA

Causes

  • Lack of vitamins in the diet – uncommon but can occur if vegan
  • Medication
  • Pernicious anaemia – this is where the immune system attacks healthy cells in the stomach which prevent the body from absorbing B12
  • Megaloblastic anaemia – develops slowly, nervous system problems
  • Impaired absorption of B12 due to intestinal diseases such as crohns, there is an intrinsic factor that binds to cobalmin and aids in its aborption in the small intesitnes
28
Q

what is the treatment for patient 2

A

Treatment

  • Treated with intramuscular hydroxocobalamin
  • Then B12 tablets may be for the red of your life
  • Vitamin B12 is found in meat, fish eggs, dairy products, yeast extracts
29
Q

what are the signs and symptoms for patient 3

A
  • Haemodialysis for renal failure
  • Exhaustion and palpitations after climbing up stairs
  • Low haemoglobin
  • Normocytic anaemia
  • Normocytic red blood cells
  • Normal white blood cell
  • Normal platelet
  • Normal reticulocytes
30
Q

what is the explanation for patient 3 and the causes

A

Explanation

  • Kidney failure
  • Usually develops in chronic renal failure due to moderlately reduced RBC life span, blood loss, inadequate increase in erythropoiesis, blood loss due to dialysis
  • EPO not stimulated

Causes

  • Chronic disease
  • Sickle cell anaemia
  • Increased destruction or loss of red blood cell
  • Uncompensated increased in plasma volume
31
Q

what are the tests and treatment for patient 3

A 
Tests
-	Kidney function test 
-	Blood film and iron tests
Treatment 
-	EPO stimulating agents should be offered to patients – can lead to uncontrolled hypertension , increase platelet count

Cardiorespiratory 2 PBL (10 decks)

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