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Year 1 - Term 2: Carriage of Oxygen > CoO PBL Condtions > Flashcards

Flashcards in CoO PBL Condtions Deck (54)
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What 2 main lung diseases does smoking cause?

How does smoke affect the lungs?

What happens if a pt quits smoking?

COPD and lung cancer

Overproduction of mucus via promotion of goblet cell growth, paralyses cilia, asthma trigger

Mucocillary clearance, goblet cell numbers decline, low FEV1 may improve, reduced risk of lung cancer (but never back to normal)


State the normal arterial Hb saturation for a healthy adult.

State 2 lung function tests that would help diagnose asthma.

How can asthma be diagnosed from other obstructive diseases e.g. COPD during lung function testing?


1. spirometry (FEV1/FVC) - <80% of predicted 2.Peak expiratory flow test (20% or more difference in PEF rate on at least 3 days in a week for at least 2 weeks)

Reversibility testing. Does breathing improve on or after administration of medication (inhaler)?


LIst 4 signs that could indicate a severe asthma attack

Define hypocapnia and explain why an asthmatic patient may have it.

1. cyanosis 2. Tachycardia 3. peak expiratory flow rate <33% 4. predicted 4. SaO2 <92%. Also silent chest, feeble respiratory effort, repiratory rate >25/min, inability to complete sentances in 1 breath

Abnormally low arterial CO2. They are breathless and hyperventilating but still have good minute ventilation and are clearing CO2 from the blood.


Name 1 class of drug that could be used for treatment of asthma and describe its main mechanism of action,

Inhaled short acting beta-2 adrenergic receptor agonist: mimics sympathetic bronchodilator action. Activates adenalate cyclase to increase cAMP andmay also reduced mediator release from inflammatory cells and airway nerves.


Inhaled corticosteroids (ICSs): antiinflamm. actions reduce oedema of airways and bronchial gland secretions thus widening airways

Muscarinic receptor antagonists: bronchodilators, blocks ACh release by parasympathetic nerves and thus blocks bronchoconstriction and hypersecretion of mucus

Orally administered leukotrine receptor antagonists


Differentiate between blue and brown asthma inhalers.

What can hypocapnia cause?

Blue: immediate rescue when experiencing symptoms like chest tightness or SoB, contains salbutamol

Brown: contain low doses of steroids that help reduce airway sensitivity. Used regularly should decrease liklihood of attacks by building up resistance to triggers.

Vasoconstriction leading to cerebral hypoxia -> transient dizziness and anxiety. Can also cause alkalosis leading to lowered plasma Ca2+ ions and increased nerve and muscle excitability = pins and needles, muscle cramps in extremities. 


What phenotypic abnormality occurs specifically in alpha thalassaemia?

Describe the term reticulocyte.

What do elevated levels in the blood film indicate and why are there raised levels in beta thalassaemia major?

Affected at birth (beta = about 6m after). Also microcytic, hyperchromic anaemia, and a decreased synthesis of the alpha Hb subunit.

Immature large RBC with reticular meshwork of rRNA but no nucleus, visible under microscope with certain stains.

Number and % of reticulocytes in blood indicate erythropoiesis level. Beta thalassaemia major: loss/destruction of mature RBC (haemolysis and resulting anaemia) accompanied by ineffective by increased prod of RBC (erythropoiesis)


What is the major form of Hb in patients with beta thalassaemia major?

Explain why a patient would have an enlarged spleen and liver.

Name 2 main forms of treatment for beta thalassaemia major.


Excessive red cell breakdown. Extramedullary haemopoiesis (outside bone medulla)


Explain the role of the following in the regulation of blood coagulation:

a) antithrombin

b) plasmin

c) prostacyclin

a) degrades serine proteases thrombin and other coagulation factors e.g. IXa, Xa, XIa and XIIa. 

b) proteolytically cleaves fibrin/inhibits excessive fibrin formation in blood clots

c) acts on platelets to prevent release of platelet granules (inhibits activation of additional platelets) if prolonged endothelial damage


How is heparin normally administered and why is this route chosen?

List 3 major signs of DVT

List 3 categories of factors that are thought to contribute to DVT

Parentally (outside of digestive tract) becuase it's not absorbed from the gut, so given in subcutaneous IV injection.

Pain, swelling, warmth (redness, engorged superficial veins)

Virchow's Triad: venous stasis, increase in blood hypercoagulability, damage to endothelial wall


What is the treatment for DVT?

What is pitting oedema?

What are some risk factor for DVT.

Start on heparin and give warfarin (2-3 days to work) once diagnosed. Check INR later and once 2-3 take off heparin and keep on warfarin. No warfarin if pregnant!

Accumulation of interstital fluid e.g. due to DVT or R sided heart failure. Pitting goes down because fluid can reenter veins. 

Age, major surgery, cancer, pregnany, oral contraceptives and HRT, inactivity, inherited


How is DVT diagnosed?

D-dimer test (fibrin degradation product present in blood after a blood clot is degrated by fibrinolysis). +ve result = abnormally high FDP in blood - has been a significant clot. -ve = unlikely you have a clot. If +ve then ultrasound (good for proximal but can't see distal too well). If DVT suspected, Well's Score also used (>2 = likley). Gold standard: contrast venography.


What is a serious complication of DVT?

Briefly describe the venous anatomy of the leg.

Pulmonary embolism.

Deep veins: dorsal venous arch -> anterior tibial. 

Medial and lateral plantar veins -> post. tibial and fibular veins.

Ant. and post tibial and fibulat unite -> popliteal -> femoreal -> external iliac

Profunda femoris -> femoral vein.

Superficial veins: dorsal venous arch -> great saphenous -> femoral

Small saphenous -> popliteal


Where does BNP originate and what is the significance of its blood level?

Why might heart failure give a raised JVP?


Secreted from ventricles when stretched, and promotes natiuresis and vasodilation. Increased levels (>100pg/ml) indicate overstretch/enlargement of ventricles and heart disease

R heart failure -> R. heart can't pump out blood delivered to it so BP buids up in veins and circulation (increasd venous hypertension)


What 2 imaging tests might be used for a patient with heart failure, and what would be seen?

X ray: heart enlargement, evidence of pulmonary oedema

Echocardiography: dilated, poorly contracted L ventricle e.g.


List 3 classes of drugs used for heart failure and explain how they work.

1) ACE-I: decrease BP and Na+ retention = decreased preload and afterload on heart. Can also use ARBs instead.

2) Beta-blockers: as long as no evidence of T2 diabetes (b/c they can block insulin release) or metabolic syndrome, decrease work of heart by decreasing contractile force

3) Diuretics: most likely loop e.g. furosemide, decrease venous blood volume, preload and workload


Heart failure can be divided into what 2 types based on ejection fraction?

1) HF due to reduced EF - systolic heart failure (EF <40%)

2) HF with preserved EF - diastolic HF


What 5 features (ABCDE) might you see on a CXR of a patient with heart failure?

A: Alveolar oedema (batwing)

B: Kerley B lines

C: Cardiomegaly

D: Dilated, prominent upper lobe vessels

E: Pleural effusion


Describe the consequences of untreated hypertension on the heart?

Describe the cause of angina.

Higher levels of arterial pressure puts mechanical stress on the arterial walls and increases heart workload, which can lead to ventricular hypertrophy. Prolonged and severe hypertension cna result in ventricular or heart failure.

Atherosclerotic obstructive coronary artery disease, restricted blood flow to myocardium and reduction in O2 delivery (hypoxia) in myocardial tissue.


Why does pain associated with stable (exertional) angina often occur in, or radiate to, the throat, neck and L upper arm?

Describe the pathology and presentation of Prinzmetal's (variant) angina.

We have no sensory awareness of internal organs. Pain fibres from the heart enter spinal cord through the posterior roots of the upper 4 thoracic nerves (T1-T4), thus pain is felt in the sensory dermatomes (or sensory receptive fields on the throat, neck, and upper arm) supplied by those spinal nerves.

Caused by vasospasm of a coronary artery. Unlike stable angina it occurs spontaneously at rest


Describe the administration and action of nitrates in the treatment of stable angina.

What role do statins play in angina?

Nitrates (e.g. glyceryl trinitrate - GTN) can be given sublingually (under tongue) with rapid absorption and uptake into blood stream. It relaxes SM -> vasodilation and increase in blood flow. Also decreases platelet aggregation.

Reduce blood cholestrol levels (and LDL) and should prevent further damage to the coronary arteries, thus reducing risk of a MI or stroke. Competitivly inhibit HMB-CoA reductase (1st enzyme of mevalonate path) used to make cholestrol.


What might you see on an ECG of a person with angina?

 ST depression


Which organs are normally first infected by TB and why?

Give the main reason why TB is difficult to treat with drugs.

What is usually the first symptom of pulmonary TB, and list 4 others that may present.

Lungs because TB prefers high levels of O2 to grow

Waxy mycolic acid capsule/CW outer layer which is v. resistant to drug penetration

First: cough. Others: weight/appetite loss, fever, night sweats, chills, cough up blood


   Give 4 methods for TB diagnosis.

What 4 drugs make up the normal 1st line treatement of TB?

What are 2 second line drugs for MDR TB?

Mantoux test. IGRA. Sputum cultures. Nucleic acid amplification tests/line probe assay. Staining (Ziehl-Neeson/Auramine)

Isoniazid, rifampicin, pyrazinamide, ethambutol.

Aminoglycoside (e.g. Amikacin), Fluoroquinolone


What is a Ghon focus?

Briefly how does TB affect the lungs once breathed in?

Ca salts deposited, seen on CXR, upper part of lower lobe or lower part of upper lobe usually.

MTB reach pulmonary alveoli -> invade and replicate in endosomes of alveolar macrophages (which attempt to eliminate it via phagocytosis with ROS and acid but it's protected by its waxy mycolic acid capsule) -> MTB eventually kills the macrophage. Other macrophages, T and B lymphocytes and fibroblasts aggregate to form granulomas and surround infected macrophages -> fuse to form ginat multinucleated cell with necrosis in centre of tubercles. Immune response supressed b/c macrophages and dendritic cells in granulomas can't present antigens to lymphocytes. During active TB if granuloma ruptures, material can be coughed up. If enters blood can establish infectious foci throughout body = milliary TB.

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