CR2 Revision 1 Flashcards
Is this heart right dominated or left dominated? [1]
right dominated
Explain what bundle branch block is [1]
Which part of ECG can see bundle branch block occur in? [1]
Explain what bundle branch block is [1]
Disruption to the electrical signal that causes your heart to beat [0.5]
Causes altered pathways for depolarisation [0.5]
Which part of ECG can see bundle branch block occur in? [1]
Prolongs QRS
Which views of the heart are seen by each type of ECG lead on a standard 12-lead ECG? [4]
- *S**eptal: V1, V2
- *A**nterior: V3, V4
- *L**ateral: V5, V6, AVL, I
- *I**nferior: II, III, AVF
AVR: neutral
Which areas of the myocardium match up with each of the coronary arteries? [4]
Left co
What is concentric hypertrophy characterised by visually? [1]
How does concentric hypertrophy occur? [1]
When does concentric hypertrophy occur? [2]
What does concentric hypertrophy cause to happen and why? [1]
What is concentric hypertrophy characterised by visually? [1]
- Increased wall thickness / reduced lumen of ventricle
How does concentric hypertrophy occur? [1]
- New sarcomeres produced
When does concentric hypertrophy occur? [1]
- Aortic stenosis
- Chronic hypertension
What does concentric hypertrophy cause to happen and why? [1]
- Decreases pre-load due to reduction in compliance (stiff)
Eccentric hypertrophy:
- Caused by? [4]
- Characterised by? [2]
Eccentric hypertrophy:
Caused by? [1]
- Aortic and mitral regurgitation
- Systolic dysfunction (loss of cardiac inotrophy
- -Volume overload (hypervolaemia due to ventricular or renal failure)
- Alcohol / cocaine
Characterised by? [2]
- Chamber dilation - lumen gets bigger, wall gets smaller: cant contract properly
Which of the following forms the right ventricle?
Truncus ateriosus Bulbus cordis Sinus venosus Primitive ventricle Primitive atria
Which of the following forms the right ventricle?
Truncus ateriosus **Bulbus cordis** Sinus venosus Primitive ventricle Primitive atria
Which of the following forms the coronary sinus?
Truncus ateriosus Bulbus cordis Sinus venosus Primitive ventricle Primitive atria
Which of the following forms the coronary sinus?
Truncus ateriosus Bulbus cordis **Sinus venosus** Primitive ventricle Primitive atria
Which of the following forms the proximal aorta and pulmonary artery?
Truncus ateriosus Bulbus cordis Sinus venosus Primitive ventricle Primitive atria
Which of the following forms the proximal aorta and pulmonary artery?
**Truncus ateriosus** Bulbus cordis Sinus venosus Primitive ventricle Primitive atria
Which of the following forms the ventricular outflow tracts?
Truncus ateriosus Bulbus cordis Sinus venosus Primitive ventricle Primitive atria
Which of the following forms the ventricular outflow tracts?
Truncus ateriosus **Bulbus cordis** Sinus venosus Primitive ventricle Primitive atria
Label this xx
What are atrial septal defects caused by? [1]
Which population seen more in? [1]
Atrial septal defect (ASD):
- not the foramen ovale failing to form!!
- caused by the septum primum and secundum failing to form: no valve, just a hole – which then cant subsequently close.
- seen 2:1 female: male
- Ductus venosus: shunts blood from WHAT to WHAT (bypassing WHAT)
- Foramen ovale: shunts blood from WHAT to WHAT (bypassing WHAT circulation)
- Ductus arteriosus: shunts blood from WHA to WHAT (bypassing WHAT)
- Ductus venosus: shunts blood from umbilical vein to IVC (bypassing liver)
- Foramen ovale: shunts blood from RA to LA (bypassing pulmonary circulation)
- Ductus arteriosus: shunts blood from pulmonary trunk to ascending aorta (bypassing lungs)
What are acyanotic heart lesions characterised by? [1]
Name 4 acyanotic heart lesions [4]
What are acyanotic heart lesions characterised by? [1]
Group of cardiac diseases with a Left-to-Right shunt or left heart abnormality which do not result in cyanosis (blue skin colour) of the baby.
Name 4 acyanotic heart lesions [4]
oASD - Atrial Septal Defects
oVSD - Ventricular Septal Defects
oPDA - Patent Ductus Arteriosus
oCoarctation of the aorta
Tetralogy of Fallot is comprimised of which 4 heart defects/
- Ventricular septal defect
- Overriding Aorta: aorta is positioned above the VSD
- Pulmonary stenosis (narrowing)
- Right ventricular hypertrophy
What is persistant truncus arteriosus? [2]
Spiral structure doesn’t form in truncus arteriosus: one common outflow tract. Both L & R ventricle pump into same outflow tract [1]
A large VSD (ventricular septal defect) below the truncal valve allows mixing of right and left ventricular blood [1]
What is transposition of the Great Vessels?
Spiral structure that separates the outflow tracts has formed, but not as a spiral – instead as a flat sheet:
- left ventricle is connected to pulm. trunk and right ventricle is connected to ascending aorta
What structures of the heart are formed from the truncus arteriosum?
Great vessels [1]
Which structures of the heart are formed from the bulbus cordis?
The smooth outfow of the left and right ventricles. The muscular right ventricle. The muscular intraventricular septum.
Which complications are associated with patent ductus arteriosus?
A small increased risk of bacterial endocarditis
Which complications are associated with a patent truncus arteriosus?
A large ventricular septal defect. Progressive heart failure. Degree of cyanosis is variable.
Describe the process of migration of neutrophils through
Process of migration:
- chemokines picked up by receptors on the neutrophils
– causes intercellular signals to get more & more neutrophils
- cause selectins (which are present on endothelial cells) and attach – endo. cells open and and squeeze through to allow enter area of inflammation
FOR HAEMATOLOGY (Blood disorders) the investigations include WHAT? [2]
FOR HAEMATOLOGY (Blood disorders) the investigations include:
Complete blood counts (CBC) or Differential blood counts to measure absolute and relative numbers of blood cells (along with morphology of cells – if required - using a drop of blood spread on a glass slide which is called a ‘blood film’ or more accurately a peripheral blood smear).
Iron, Ferritin and Tranferrin levels, B12 and Folic acid levels: used to make Hb - can indicate anaemias
What are the two methods for classifying leukemia? [2]
What are the two methods for classifying leukemia? [2]
- Acute: abnormal cells are immature - multiply rapidly and disease worsens quickly. Commonly children
- Chronic: abnormal cells are mature - can normally function for a while so can be undiagnosed for years. Mostly adults
- Lymphocytic: Lymphoid cells affected. These make up immune system
- Myelogenous: Affects myloid cells (bone), including rbc and wbc and platelet producing cells
How would you ID acute myeloid leukemia? (AML)
- A heterogeneous population of myeloblasts with cells ranging from small to medium-sized to large. Note presence of a few maturing myeloid elements.
- Large myeloblasts with prominent nucleoli. Maturing myeloid elements i.e. neutrophils or eosinophils.
How would you ID chronic lymphocytic leukemia (CLL) from PBS and BMS?
- PBS: Mature-appearing lymphocytes with high nuclear to cytoplasmic ratios, with scant agranular cytoplasm and homogeneously condensed chromatin without nucleoli. Characteristic “soccer ball’ chromatin pattern. Numerous smudge cells
- BMS: tissue is displaced by nodular and interstitial aggregates of clonal B cells.
How would you ID chronic myeloid leukemia (CML) from PBS and BMS?
PBS: > 100K white blood cells with neutrophilia, significant increase in metamyelocytes and myelocytes, also basophilia and eosinophilia
BMS: increased granulocyte precursors, basophils, eosinophils and occasionally monocytes
Normal erythroid compartment, variable pseudo Gaucher cells and sea blue histiocytes, increased reticulin fibres
Describe the process of migration of neutrophils through
Process of migration:
- chemokines picked up by receptors on the neutrophils
– causes intercellular signals to get more & more neutrophils
- cause selectins (which are present on endothelial cells) and attach – endo. cells open and and squeeze through to allow enter area of inflammation
FOR HAEMATOLOGY (Blood disorders) the investigations include WHAT? [2]
FOR HAEMATOLOGY (Blood disorders) the investigations include:
Complete blood counts (CBC) or Differential blood counts to measure absolute and relative numbers of blood cells (along with morphology of cells – if required - using a drop of blood spread on a glass slide which is called a ‘blood film’ or more accurately a peripheral blood smear).
Iron, Ferritin and Tranferrin levels, B12 and Folic acid levels: used to make Hb - can indicate anaemias
What are the two methods for classifying leukemia? [2]
What are the two methods for classifying leukemia? [2]
- Acute: abnormal cells are immature - multiply rapidly and disease worsens quickly. Commonly children
- Chronic: abnormal cells are mature - can normally function for a while so can be undiagnosed for years. Mostly adults
- Lymphocytic: Lymphoid cells affected. These make up immune system
- Myelogenous: Affects myloid cells (bone), including rbc and wbc and platelet producing cells
How would you ID acute myeloid leukemia? (AML)
- A heterogeneous population of myeloblasts with cells ranging from small to medium-sized to large. Note presence of a few maturing myeloid elements.
- Large myeloblasts with prominent nucleoli. Maturing myeloid elements i.e. neutrophils or eosinophils.
How would you ID chronic lymphocytic leukemia (CLL) from PBS and BMS?
- PBS: Mature-appearing lymphocytes with high nuclear to cytoplasmic ratios, with scant agranular cytoplasm and homogeneously condensed chromatin without nucleoli. Characteristic “soccer ball’ chromatin pattern. Numerous smudge cells
- BMS: tissue is displaced by nodular and interstitial aggregates of clonal B cells.
How would you ID chronic myeloid leukemia (CML) from PBS and BMS?
PBS: > 100K white blood cells with neutrophilia, significant increase in metamyelocytes and myelocytes, also basophilia and eosinophilia
BMS: increased granulocyte precursors, basophils, eosinophils and occasionally monocytes
Normal erythroid compartment, variable pseudo Gaucher cells and sea blue histiocytes, increased reticulin fibres
Left-sided heart failure results in blood backing up into the lungs, what condition can this lead to? [1]
Acceptable responses: oedema, pulmonary oedema, pulmonay edema, edema
What happens as a result of right sided heart failure? [1]
As the blood drains into the right side of the heart from the systemic circulation, the blood therefore backs up into the rest of the body altering the pressure
Which of the following conditions would cause eccentric hypertrophy [2]
Renal failure
Aortic stenosis
Aortic regurgitation
Increased BP
Which of the following conditions would cause eccentric hypertrophy [2]
Renal failure
Aortic stenosis
Aortic regurgitation
Increased BP
*Eccentric hypertrophy is caused by volume overload, so could be caused by renal failure (which increases blood volume). It could also be caused by valve regurgitation.
Aortic stenosis usually results in initial concentric hypertrophy, but this in itself can then leads to eccentric hypertrophy.*
What is shown here?
Kerley B Lines
These are thin lines, often of no more than a couple of centimetres often found towards the base and peripheral regions of the lung where the interstitial has thickened. They lie at 90o to the pleura. On the image, some of these lines are present towards the base of the right lung.
What condition is shown here?
Upper Lobe Blood Diversion
Due to the increased pressures, blood is pushed upwards creating a ‘stag antler’ appearance. Blood is diverted as fluid is more likely to build up lower down due to gravity and cause relative hypoxia and vasoconstriction, thus the blood is diverted to the upper zones.
In the midline of this film, we can also see several sternal sutures.
At what time does ductus arteriosus normally close?
Seconds after birth
1-3 days after birth
2 weeks after birth
6 months after birth
At what time does ductus arteriosus normally close?
Seconds after birth
1-3 days after birth
2 weeks after birth
6 months after birth
Explain the mechanism of iron absorbtion and transport in the body for haem iron and non haem iron
Haem iron
- Haem iron – (highly bioavailable) absorbed through DMT1
- Fe removed from Haem. Can then be stored as ferritin OR can exit cell through Ferroportin
Non-haem iron:
- Mostly in the form of Fe3+, but only Fe2+ can be absorbed by the enterocyte. Enzyme reductase: Fe3+ à Fe2+
- Enters via DMT1
- Fe removed from Haem. Can then be stored as ferritin OR can exit cell through Ferroportin
Then transferrin transports Fe3+ around body
How do we store iron in body? [1]
Where is this mostly occuring? [1]
What is clinicially signficicant about having inflammation and 1? [1]
How do we store iron in body? [1]
Via ferritin (storage protein): hence low serum ferritin is an important diagnostic test for iron deficiency anemia
Where is this mostly occuring? [1]
Liver:
What is clinicially signficicant about having inflammation and 1? [1]
ferritin is released into the blood during inflammation
THEREFORE can miss deficiency have if high inflammation
What is the first committed cell in erythropeoisis? [1]
What is the pathway from Haematopoietic stem cell (HPSCs) - to erythrocyte? [1]
What is the first committed cell in erythropeoisis? [1]
Proerythroblast
Haematopoietic stem cell (HPSCs) –> common myeloid progenitor cell –> (CMPC)Proerythroblast –> erythroblast –> reticulocyte – > erythocyte
The proerythroblast develops into an (early) erythroblast. The erythroblast then undergoes a sequence of changes where its nucleus progressively shrinks and its cytoplasm becomes filled with haemoglobin (not stained). When full of haemoglobin it is called a normoblast. The normoblast then expels its nucleus and becomes a reticulocyte. Most reticulocytes stay in the marrow and mature into erythrocytes but some may be released into the blood, especially after haemorrhage. Reticulocytes can transport oxygen, just not as efficiently as mature erythrocytes. They can mature into adult RBCs in the circulation
Explain the mechanism of how Fe is recylced during rbc breakdown?
Explain the mechanism of how Fe is recylced during rbc breakdown?
splenic macrophages break down old rbc, via action of haem oxygenase.
Fe3+enters circulation carried ontransferrinto be re-used and exits viaferroportin
Describe the mechanism of haem degredation [5]
(Iron has already been recycled)
- Haem turns into unconjugated bilirubin
- Liver takes up unconjugated bilirubin, and via bilirubin diglucoronide is conjugated with glucoronic acid
- sent to gall bladder and stored in bile
- goes to gut after secreted.
- bilirubin converted to urobilinogen and then oxidised to stercobilin & excreted in faeces. some urobilinogen is converted to urobilin and excreted in urine
What are specific signs associated with anaemia of iron deficiency? [2]
What are specific signs associated with anaemia of vit. B12 deficiency? [1]
What are specific signs associated with anaemia of thelessasmia? [1]
What are specific signs associated with iron deficiency? [2]
- Koilonychia (spoon shaped nails)
- Angular stomatitis (inflammation of corners of mouth)
What are specific signs associated with anaemia of vit. B12 deficiency? [1]
Glossitis (inflammation of tongue)
What are specific signs associated with anaemia of thelessasmia? [1]
abnormal bone facial development
What is urgent to eliminate if you have patient 60+ and has iron deficiency anaemia? [1]
What is urgent to eliminate if you have patient 60+ and has iron deficiency anaemia? [1]
Check for colon cancers / GI malignancy
What is anaemia of inflammation / chronic disease caused by? [3]
Why will iron supplementation not help in patients with this condition?
What is anaemia of inflammation?
IL-6 released and causes:
* more hepcidin: which blocks release of Fe2+ out of via ferroportin
* blocks production of EPO (& therefore rbc production)
* inhibits production of rbc in bone marrow
Why will iron supplementation not help in patients with this condition?
Problem is with iron being absorbed in gut and iron getting out of macrophages, along with depressed erythropoietin release and erythropoiesis caused by inflammatory cytokines – need to treat cause inflammation
Explain what elevated erythrocyte Sedimentation Rate test indicates [1]
Elevated sedimentation rate (ESR) indicates inflammation – can be secondary to infection, auto-immune illness – different labs will have slightly different normal ranges
- Erythrocytes have negative surface charge*
- Ensures that they electrostatically repel each other and do not stick together, particularly in capillaries.*
- Inflammatory cytokines or bacteria in blood increase amount of (positively charged) fibrinogen in plasma*
- Excess fibrinogen binds to red cell membrane and reduces its negative charge, causing RBCs to adhere*
- Therefore, rate of sedimentation increases as clumps of RBCs fall down through test tube more quickly.*
Explain how B12 [1] and folate deficiencies [1] would affect the NS?
Which pathology would B12 deficiency lead to if left untreated? [1]
- Folate deficiency: neural tube defects
- B12 deficiency: demylination:
if not treated can lead to: subacute combined degeneration of the cord
Degeneration of posterior and lateral columns of spinal cord: TEST FOR WITH ROMBERG SIGN
How do you diagnose megaloblastic anaemia from a PBS? [1]
What is elevated for when evaluating megaloblastic anaemia bloods? [3]
What should you also test for alongside a full blood count for megaloblastic anaemia? [2]
Diagnostic cell on smear for megaloblastic anaemia is hyper-segmented neutrophils: 6 or more lobes
Also elevated:
* MCV
* serum ferritin (bc is a type of inflammation)
* plasma lactate dehydrogenase
What should you also test for alongside a full blood count for megaloblastic anaemia? [2]
* vit. B12 level
* serum folate lvls / rbc folate levels
(but Serum vitamin B12 blood test can be unreliable so repeat if borderline , a low ”normal” B12 level does not rule out B12 deficiency!
If levels indeterminate check plasma total homocysteine (tHcy) and/or plasma methylmalonic acid (MMA)
Treatment for folate deficiency? [1]
Treatment for vitamin B12 deficiency:
- pernicious anaemia? [1]
- alternative causes? [1]
Folate: oral folic acid
B12:
- for pernicious anaemia: hydroxycobalamine IM (NOT ORAL). be aware of hypokalaemia due to increased K+ requirement as erypoesis increase back to normal
- other: Oral cyanocobalamine
What is haemolytic anaemia? [1]
What are the classifications? [2] State all of each
What are the key lab findings to show haemolytic anaemia? [3]
What is haemolytic anaemia? [1]
abnormal breakdown reduces lifespan of rbc
What are the two types? [2]
Inherited (defetive gene):
* .glycolysis defect
* pentose p pathway (generates NADPH - which involved in anti-oxidants for rbc)
* membrane protein defects
* SCA
Acquired:
* heat damage
* mech damage
* antibody damage
What are the key lab findings to show haemolytic anaemia? [3]_
Raised: reticulocytes, bilirubin (breakdown of haem) & LDH
what are symptoms of haemolytic anaemia? [3]
Will depend on time frame of haemolysis:
Jaundice
- more rbc being produced, more bilirubin is made as a product of more haem breakdown.
- This can lead to pigment gallstones High bilirubin causes yellowish discolouration of skin & sclera of eye
Splenomegaly
- extramedullary hematopoiesis (“making blood” outside bone marrow) in red pulp spleen.
Massive sudden haemolysis
- e.g. from incompatible blood transfusion can cause cardiac arrest due to lack of oxygen delivery to tissues & hyperkalaemia due to release of intracellular contents) Urine dark colour due to conjugated bilirubin
What is pernicious anaemia caused by?
Autoimmune antibodies to parietal cells (sensitive) or IF (specific) – destroy or inactivate IF: SO:
Decreased or absent Intrinsic factor (IF) causes progressive exhaustion of B12 reserves.
How can folate mask B12 defiency?
Elevated intake of folic acid alleviates anaemia caused by B12 deficiency by providing a continual supply of active folate (otherwise B12 needed to regenerate active folate via methionine synthase). BUT irreversible neurological sequelae B12 deficiency may still occur!
Name & explain 2 inherited defects that cause haemolyitc anaemia, arising from enzymes? [2]
Pyruvate Kinase Deficiency:
- Causes deficiency in pyruvate kinase in erythrocytes: final step in glycolysis
- Less energy for ATPase pump – cells lose K+ & H20, dehydrate and are destroyed - haemolysis
Pentose Phosphate Pathway: Glucose-6-phosphate dehydrogenase (G6PD) deficiency:
- NADPH required to keep glutathione in reduced state – major cellular anti-oxidant
- Pentose phosphate pathway is only source of reduced glutathione in RBC – so RBCs very affected when exposed to oxidative stress
- Increased oxidative stress from infection or drugs (examples, sulfa drugs, primaquine) or certain foods (one example, fava beans) will cause haemolysis
Haemolytic anaemias:
Explain how can get aquired damage to RBC?
Microangiopathic haemolytic anaemia: from mechanical damage:
- stress from passing through heart valves
- cells snag on fibrin strands
- heat damage
- osmotic damage (drowing in freshwater)
ALL TYPES OF INTRAVASCULAR HAEMOLYSIS
GO OVER THE CYCLE in lecture
Label A
Heinz Bodies
