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Yr 2 EOYS ^2 > CR EOYS1 > Flashcards

CR EOYS1 Flashcards

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1
Q

Decsribe the structure of NOSs xx

A

NOS: oxidoreductase homodimer enzymes:

  • Oxygenase domain: binding for NADPH, FMN & FAD
  • Reductase domain: binding for BH4, heme and L’arginine (substrate
  • Calmodulin binding site: in between reductase and oxidase domains
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2
Q

What happens to NOS if there is / isn’t BH4 present?

A

BH4 present: causes dimerisation and proper catalytic activity for NO formation

BH4 absence: causes monomer, becomes a superoxide

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3
Q

For the formation of NO using NOS, what substrates are essential? [3]

Which co-factors are essential? [5]

A

For the formation of NO using NOS, what substrates are essential? [3]
- L-arginine
- O2
- NADPH

Which co-factors are essential? [5]
- FAD
- FMN
- BH4
- haem
- calmodulin.

OXYGEN is essential for the synthesis. Because of the oxygen requirement, NO synthesis is inhibited in hypoxic tissue

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4
Q

Explain MoA of endothelial NO synthase creating NO

A
  • Normally: eNOS associates with Caveolin 1 in caveolae (invaginations of plasma membrane) this inhibits calmodulin complex (CaM) binding to eNOS
  • Shear stress promotes wall stretching, which promotes the dissociation of eNOS from caveolae
  • This allows eNOS release into the cytoplasm and its activation (through binding of a Ca2+/ calmodulin (CaM) complex)
  • M2-muscarinic acetylcholine receptor activation or other stimulation initiates an influx of Ca2+ that binds to calmodulin.
  • eNOS dissociates from Cav1 and then combines to Ca/CaM.
  • eNOS is activated leading to synthesis of NO.
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5
Q

[] shear stress favors the activation of eNOS by releasing endothelium-dependent agonists.

What are they? [4]

A

Increased shear stress favors the activation of eNOS by releasing endothelium-dependent agonists.

Agonists stimulated NO formation:
* Acetylcholine (M3muscarinic)
* Bradykinin
* Substance-P
* Adenosine

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6
Q

What can endothelial dysfunction be caused by? [4]

A

Consumptive processes that transform bioavailable NO into other species:

  • Reactive oxygen species such as -O2 reacts readily with NO forming peroxynitrite (ONOO−)
  • Uncoupling of NOS: BH4 insufficiency results in uncoupled NOS, which produces superoxide anions instead of NO

Deficiencies in production of NO in the endothelium:
- Reduced bioavailability of l-arginine o
- Presence of its inhibitor, asymmetric dimethyl-l-arginine (ADMA)

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7
Q

Describe the pathophysiology behind acute bronchitis (e.g. caused by respiratory synctial virus)

A

Epithelial cells: 1st line of defence

RSV: binds and invades mucosal lining via epithelial cells

Epithelial cells switch on immune response after recognised through Toll-like receptor (TLR)-3 and retinoic acid-inducible gene (RIG)-I-like receptors

Cellular infection triggers the release of early inflammatory mediators (e.g.interferons (IFNs) and tumour necrosis factor (TNF)-α) and chemokines (e.g.CXCL8 and CXCL11).

A) Innate: Macrophages and Neutrophils, e.g. PMN polymorphonuclear leukocytes cells recruited PMNs)

B) Acquired: Dendritic cell, triggering B and T cells: CD4, CD8 and primed T cells

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8
Q

Name the signs of pneumonia [4]

Name a complication that pneuomonia a risk factor for !!

A

Signs:
- Tachypnoea
- Tachycardia
- Hypoxia
- Hypotension
- Fever
- Confusion

Can lead to sepsis

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9
Q

How do you diagnose acute bronchitis?

A

Diagnosis by exclusion:

  • Cough >3 weeks
  • If signs of consolidation (on CXR), airway obstruction, fever, increase RR, increase HR: NOT acute bronchitis
  • If no: is there currently an outbreak of influenza pertusis (whooping cough)?
  • If no: Acute bronchitis
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10
Q

How does hypertension damage the heart?

What effect does HTN have on SVR? [1]
State the cardiac remodelling that initially occurs because of HTN [1]
State the effect on heart performance of chronic HTN [2]

A

HTN leads to increased systemic vascular resistance compared to normal in HTN.

Initially leads to HTN leads toleft ventricular hypertrophy (initially protective, but long term is damaging) to overcome increased afterload:

Chronic HTN leads to diastolic and (eventually) systolic dysfunction: there is less space to in ventricle to pump blood out. This leads to dilated cardiomyopathy/congestive heart failure

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11
Q

what can left ventricular hypertrophy lead to? [3]

A

Dilated cardiomyopathy/congestive heart failure

If increased cardiac muscle is not well perfused myocardial ischaemia and myocardial infarction can follow.

Conducting system also impacted: increasing risk arrythmias

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12
Q

What are the BP ranges for isolated diastolic HTN (BP)? [1]

A

Abstract. In various guidelines, isolated diastolic hypertension is defined as diastolic blood pressure >80 or >90mmHg in individuals with normal systolic blood pressure.

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13
Q

Why does obesity increase BP? [3]

A
  • increased oxidative stress damages endothelium of BV: stiffer
  • increased RAAS system
  • increases sympathetic system

which all influence CVD and CKD, which themselves contribute to BP

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14
Q

What specifically about obesity causes increase in HTN? [1]

A

High leptin levels increase activity of RAAS and sympathetic NS

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15
Q

Anti-hypertensives:

Which of the following class of drug does indapamide fall into?

ACE inhibitors:
Angiotensin-II receptor antagonists
Calcium-channel blocker
Diuretics
Beta-blockers

A

Which of the following class of drug does indapamide fall into?

ACE inhibitors:
Angiotensin-II receptor antagonists
Calcium-channel blocker
Diuretics thiazide-like diuretic
Beta-blockers

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16
Q

Which of the following class of drug does enalapril fall into?

ACE inhibitors:
Angiotensin-II receptor antagonists
Calcium-channel blocker
Diuretics
Beta-blockers

A

Which of the following class of drug does enalapril fall into?

ACE inhibitors:
Angiotensin-II receptor antagonists
Calcium-channel blocker
Diuretics
Beta-blockers

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17
Q

Which of the following class of drug does losartan fall into?

ACE inhibitors:
Angiotensin-II receptor antagonists
Calcium-channel blocker
Diuretics
Beta-blockers

A

Which of the following class of drug does losartan fall into?

ACE inhibitors:
Angiotensin-II receptor antagonists
Calcium-channel blocker
Diuretics
Beta-blockers

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18
Q

Which of the following would you use to deliver 24 – 30% O2 (maximum flow rate of 4L/min) for mild hypoxia?

Nasal cannulae
Simple face mask
Non-rebreather mask
Venturi mask

A

Which of the following would you use to deliver 24 – 30% O2 (maximum flow rate of 4L/min) for mild hypoxia?

Nasal cannulae
Simple face mask
Non-rebreather mask
Venturi mask

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19
Q

Which of the following would you use to deliver for patients with chronic obstructive pulmonary disease (COPD) due to the risk of type 2 respiratory failure.

Nasal cannulae
Simple face mask
Non-rebreather mask
Venturi mask

A

Which of the following would you use to deliver for patients with chronic obstructive pulmonary disease (COPD) due to the risk of type 2 respiratory failure.

Nasal cannulae
Simple face mask
Non-rebreather mask
Venturi mask

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20
Q

Which of the following would you use to deliver approximately 70% O2 when used with a 15L oxygen flow rate.

Nasal cannulae
Simple face mask
Non-rebreather mask
Venturi mask

A

Which of the following would you use to deliver approximately 70% O2 when used with a 15L oxygen flow rate.

Nasal cannulae
Simple face mask
Non-rebreather mask
Venturi mask

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21
Q

7Which of the following would you use to deliver 30 – 40% O2 (flow rate 5-10 L/min)

Nasal cannulae
Simple face mask
Non-rebreather mask
Venturi mask

A

Which of the following would you use to deliver 30 – 40% O2 (flow rate 5-10 L/min)

Nasal cannulae
Simple face mask
Non-rebreather mask
Venturi mask

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22
Q

Which of the following would used to treat patients with a significant degree of hypoxia (moderate to severe).

Nasal cannulae
Simple face mask
Non-rebreather mask
Venturi mask

A

Which of the following would used to treat patients with a significant degree of hypoxia (moderate to severe).

Nasal cannulae
Simple face mask
Non-rebreather mask
Venturi mask

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23
Q

What mmHg would systolic [1] and diastolic [1] blood pressure indicate have pneumonia? [2]

A
  • SBP < 90
  • DBP < 60
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24
Q

The larynx lies in which vertebral layers? [1]

25
The vocal cords attach posteriorly to which of the following? Cricoid cartilage Cuneiform cartilage Epiglottis Arytenoid cartilage Thyroid cartilage
The vocal cords attach posteriorly to which of the following? Cricoid cartilage Cuneiform cartilage Epiglottis **Arytenoid cartilages** Thyroid cartilage
26
Palsy to which nerve causes reduced gag reflex? Superior laryngeal nerve, external branch Superior laryngeal nerve, internal branch Recurrent layngeal nerve, bilateral damage Recurrent layngeal nerve, unilateral damage
Palsy to which nerve causes reduced gag reflex? **Superior laryngeal nerve, internal branch**
27
Why is DCLO raised in asthma Ptx?
Expiration is decreased, so air is trapped in the lungs. Have a lot of blood vessel recruitment
28
How do you calculate VO2? [1] What is the name of the equation? [1]
Fick equation: **VO2 = Q x (CaO2-CvO2)** Q is the cardiac output of the heart (blood flow to muscle) CaO2 is the arterial oxygen content CvO2 is the venous oxygen content (CaO2 – CvO2) is also known as the arteriovenous oxygen difference.
29
What happens to the levels of paO2 in arterial blood during high levels of exercise?
At high levelss of exercise the paO2 in the **arterial blood declines slightly**
30
During exercise, changes in autonomic factors (inhibition of parasympathetic and increase in sympathetic) are controlled by WHAT?
**Central command**: area in brain that mediates autonomic responses (increase in sympathetic / decrease in parasympathetic) to exercise. **Happens at same time as brain tells muscles to move**: e.g. The increase in heart rate, even within the first beat, is proportional to the force developed Once begun, chemical and metabolic tweaks to the system: chemoreceptors, baroreceptors
31
What would DCLO be expected to be in COPD & asthma patients? DCLO reduced in COPD & asthma patients DCLO reduced in COPD but raised in asthma patients DCLO reduced in asthma but raised in COPD patients DCLO raised in COPD and asthma patients
What would DCLO be expected to be in COPD & asthma patients? DCLO reduced in COPD & asthma patients **DCLO reduced in COPD but raised in asthma patients** Low KCO: seen in COPD with emphysema due to **alveolar destruction** (usually normal in chronic bronchitis) with an obstructive pattern on PFT. DCLO reduced in asthma but raised in COPD patients DCLO raised in COPD and asthma patients
32
A 69-year-old male presents with pleuritic chest pain and shortness of breath. He is normally fit and well. On examination, he is alert, orientated and conversing with you. He is febrile (38.4) and tachycardic (105bpm) but other observations are within normal limits. A chest x-ray demonstrates left lower zone consolidation. Blood tests are as follows: Urea: 8mmol/L Creatinine: 115 µmol/l WCC: 13 10^9/l Hb: 130 g/l An ECG is performed showing sinus rhythm with some ventricular ectopics. A diagnosis of community-acquired pneumonia is made. What is this patient’s CURB-65 score? 3 2 4 1 5
**2** CURB-65 is a scoring system used to grade the severity of pneumonia: Confusion Urea > 7 Respiratory rate ≥ 30 Blood pressure <90mmHg systolic or ≤60mmHg diastolic Aged ≥ 65 years old
33
Which of the following is the correct name for the piece of equipment shown in the image? Nasal cannulae Venturi mask Nasopharyngeal airway Reservoir mask Hudson mask
Which of the following is the correct name for the piece of equipment shown in the image? Nasal cannulae Venturi mask Nasopharyngeal airway **Reservoir mask** Hudson mask
34
Which of the following treatments of pneumonia causes toxic optic neuropathy? Rifampicin Isoniazid Ethambutol Pyrazinamide
Which of the following treatments of pneumonia causes toxic optic neuropathy? Rifampicin Isoniazid **Ethambutol** Pyrazinamide
35
An 82-year-old lady presents to the hospital with a fever and confusion. A CXR is performed showing a right-sided basal pneumonia. Her blood tests reveal a urea of 12mmol/L. Her observations are shown below: Oxygen saturation 94% on air Heart rate 120 bpm Blood pressure 110/57 mmHg Respiratory rate 28 breaths per minute Temperature 38.1oC What is her CURB 65 score? 2 3 5 4 1
An 82-year-old lady presents to the hospital with a fever and confusion. A CXR is performed showing a right-sided basal pneumonia. Her blood tests reveal a urea of 12mmol/L. Her observations are shown below: Oxygen saturation 94% on air Heart rate 120 bpm Blood pressure 110/57 mmHg Respiratory rate 28 breaths per minute Temperature 38.1oC What is her CURB 65 score? 2 3 5 **4** 1 **She would score for confusion, urea, diastolic blood pressure and age, bringing her total score to 4.**
36
A 36-year-old Norwegian female presents with a 4-month history of gradually progressive shortness of breath, a non-productive cough and fatigue. She also reports painful red lesions on her shins. She has no significant medical/surgical history and is on no regular medications. She has no family history of note. She is a non-smoker and non-drinker. She is married and works as a classroom assistant. Her review of systems is otherwise unremarkable. She is afebrile and her vital signs are within normal limits. Respiratory examination is normal. On inspection of the lower limbs, there are tender erythematous nodules on the anterior aspects of her lower legs bilaterally. Given the most likely underlying diagnosis, what is the most likely cause of the skin lesions on her lower limbs? Necrobiosis lipoidica Pyoderma gangrenosum Acanthosis nigricans Erythema multiforme Erythema nodosum
**Erythema nodosum** The most likely underlying diagnosis is sarcoidosis, given this patient's Scandinavian ancestry, age, female gender and constellation of non-specific symptoms and signs. Erythema nodosum (painful, blue-red nodules most commonly affecting the shins) is associated with sarcoidosis. Other causes of erythema nodosum include TB, streptococci and certain drugs (eg. sulfonamides, dapsone, COCP).
37
Which of the following is not part of Weldeyer ring? Pharyngeal Tubal Lingual Tonsular Palatine
Which of the following is not part of Weldeyer ring? Pharyngeal Tubal Lingual **Tonsular** Palatine
38
What is the earliest and most notable physiological change seen in patients experiencing hypovolemic shock? TachypneaTachypnea Hypotension Altered mental status Tachycardia
Tachycardia
39
Which of the following conditions does not contribute to shock by increasing tissue demand for oxygen and nutrients? Pain FeverIncorrect response Infection Respiratory distress
Respiratory distress
40
750 - 1500 ml of blood loss would indicate which stage of shock? Class I Class II Class III Class IV
750 - 1500 ml of blood loss would indicate which stage of shock? Class I **Class II** Class III Class IV
41
< 750ml of blood loss would indicate which stage of shock? Class I Class II Class III Class IV
**Class I**
42
1500 - 2000 ml of blood loss would indicate which stage of shock? Class I Class II Class III Class IV
1500 - 2000 ml of blood loss would indicate which stage of shock? Class I Class II **Class III** Class IV
43
> 2000 ml of blood loss would indicate which stage of shock? Class I Class II Class III Class IV
**Class IV**
44
Explain three examples that could cause obstructive shock xx [2]
**PE** **Tension pneuomothorax** air gets trapped in pleural space: compresses against vena cava and heart: stops blood flow into right side of heart: reduced preload: reduced CO **Cardiac tamponade** :accumulation of pericardial fluid: causes increas in intrapericardial pressure which reduceds cardiac filling
45
Explain 3 examples of distributive shock x
**Sepsis**: dysregulated host response to infection where bacteria in blood release chemicals causing uncontrolled hypotension **Anaphylactic shock**: allergic response to antigen: IgE mediated mass degranulation releasing histamines: **vasodilation and capillary leaking** **Neurogenic shock:** loss of sympathetic tone and thus unopposed parasympathetic response driven by the vagus nerve. Consequently, patients suffer from instability in blood pressure,
46
What is cardiogenic shock? Name 4 causes of cardiogenic shock xx [4]
Failure of the heart to pump blood Occurs as a result of ventricular dysfunction (esp. LV) **Causes**: * Acute myocardial infarction leading to ventricular dysfunction * Arrhythmias * Valvular rupture * Decompensated heart failure
47
Explain the compensatory mechanisms for haemorrhagic shock [3]
Baroreceptors detect drop in arterial pressure Activates sympathetic stimulation: - **Constriction of small arterioles** increasing total peripheral resistance thereby maintaining BP - **Veins and venous reservoirs constrict**, maintaining venous return - **Increased heart rate and contractility** to maintain **cardiac output** CNS ischaemia results in increased **noradrenaline and adrenaline** secretion from adrenal medulla
48
Name 3 long term compensatory mechanisms of shock [3]
- There is (by an unknown mechanism) stimulation of **albumin** and other plasma protein synthesis in the liver. - **Increased fluid absorption from GI tract** - Fibroblasts surrounding the kidney tubules are sensitive to hypoxia and release increased amounts of **erythropoietin: Red cell production**
49
CO = [] X []? BP = [] x []?
CO = **HR X SV** BP = **CO x Systemic vascular resistance**
50
What are the overall physiological consequences of shock ? [3]
- **Increased afterload** - **Reduced systemic vascular resistance** (Failure to maintain peripheral vasoconstriction) - **Decreased CO** i) reduced preload ii) reduced contactility
51
Describe the 4 classes of haemorrhagic shock
x
52
What is waldeyers ring? [4]
Waldeyer's ring consists of four tonsillar structures: - **pharyngeal** - **tubal** - **palatine** - **lingual** As well as small collections of lymphatic tissue disbursed throughout the mucosal lining of the pharynx (mucosa-associated lymphoid tissue, MALT).
53
What are the axillary lymph nodes? [3] Where do they drain lymph from? [3] Ddescribe their path to to L / R venous angle [2]
**Humeral** lymph nodes drain from **upper limb** **Pectoral** lymph nodes drain from **anterior chest wall** (majority drains into here) **Subscapular** lymph nodes drain from **posterior chest wall** (rotator cuffs etc) Together: go to **central** --> **apical** --> **supraclavicular** --> **left / right venous angle**
54
Label the vert. layers of A-D
55
The laryngeal prominence occurs at which vertebral level C3 C4 C5 C6 C7
The laryngeal prominence occurs at which vertebral level C3 **C4** C5 C6 C7
56
The carotid bifurication occurs at which vert. level? C3 C4 C5 C6
The carotid bifurication occurs at which vert. level? C3 **C4** : **carotid pulse can be palpated either side of thyroid cartilage** C5 C6
57
The cricoid cartilage occurs at which vert. level? C3 C4 C5 C6
The cricoid cartilage occurs at which vert. level? C3 C4 C5 **C6**
58
The thyroid gland occurs at which vert. level? C3 C4 C5 C6
The thyroid gland occurs at which vert. level? C3 C4 C5 **C6**: overlies cricoid cartilage
59
Thyroid gland overlies which laryngeal cartilage? Thyroid cartilage Cricoid cartilage Epiglottis Artyenoid cartilages
Thyroid gland overlies which laryngeal cartilage? Thyroid cartilage **Cricoid cartilage** Epiglottis Artyenoid cartilages

Yr 2 EOYS ^2 (42 decks)

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