BDS 2 MCQ bioscience

what does HIV cause?

opportunistic infections

secondary to severe impairment of cell-mediated immunity

how is HIV transmitted?

blood- parenteral/ intravenous drug user

bodily fluids- sexual transmission; baby delivery/ breastfeeding

how to treat HIV if suspected exposure?

PEP- 4-72 hours after

How does HIV bind to host cells?

CD4+ Th receptors

replication of HIV

1. bind to CD4+ Th receptors on host cells

2. reverse transcriptase converts viral RNA —> DNA

3. integration to host DNA

4. genome packaged in protein coat by proteases

5. release of mature virus—> infects other cells

universal precaution of HIV

everyone is presumed to have HIV until proven otherwise

opportunistic infections caused by defective cell-mediated immunity caused by HIV

• intracellular pathogens

myobacter

—> TB

opportunistic infections caused by defective cell-mediated immunity caused by HIV

• viruses

cytomegalovirus

varicella zoster—> chicken pox—> shingles

opportunistic infections caused by defective cell-mediated immunity caused by HIV

• fungal

meningitis

oral candidiasis

opportunistic infections caused by defective cell-mediated immunity caused by HIV

• protazoal

cerebral toxoplasmosis

opportunistic infections caused by defective cell-mediated immunity caused by HIV

• cancers

kaposi’s sarcoma- gumline/ roof of mouth

HPV

classification of HIV

<200 CD4+ Th

dental symptoms of HIV

• angular chelitis- fungal

• glossitis

• candida

• oral hairy leukoplakia

• gingivitis

• parotitis

• kaposi’s sarcoma on gumline/ roof of mouth

• oral ulcers

roughly how long does HIV stay latent?

10 yrs

what are long-term non-progressors?

stay in latent phase of HIV

when are you cured of HIV?

HIV RNA undetectable

how does BIKTARVY treat HIV?

targets HIV replication cycle

increases immune system

side effect of BIKTARVY to treat HIV

induce/ inhibit Cytochrome P450

= subtherapeutic/ toxic levels of oral sedatives e.g. medazolam

test for HIV

antibody HIV + P24 antigen

• current infection

what is window period?

takes up to 3 months to make HIV

what is anatomical dead space?

respiratory system volume excluding the alveoli

function of anatomical dead space

transports air to alveoli to stop big changes in CO2

ventilation inefficiency

25% of air stays in airways

not all air inspired used for gas exchange

tidal volume

500mls

what is alveolar dead space?

lung disease

• alveolar not acting as respiratory membrane

what is physiological dead space?

anatomical + alveolar dead space

• areas not involved in gas exchange

circulatory inefficiency

difference in alveolar and circulation pO2 due to venous shunting

what is alveolar pO2?

104mmHg

what is circulatory pO2?

95mmHg

where is venous shunting present?

bronchial circulation: deoxygenated blood from airways to left atrium

pulmonary circulation: deoxygenated blood from thebesian veins of heart to left ventricle

what is required for efficient gas exchange?

good match between alveolar ventilation (Va) and blood flow (Q)

what happens to Va/ Q when

• embolus/ vasoconstriction?

decreased blood flow (Q)

• increased alveolar dead space

what happens to Va/ Q when

• mucus plug/ pneumothorax/ broncoconstriction?

decreased alveolar ventilation (Va)

• increased alveolar dead space

consequences of hypoxia

close O2 sensitive K+ channels

induced vasoconstriction of pulmonary arteries

increased pulmonary pressure in pulmonary arteries

cor pulmonale

what happens to Va/ Q when

• underventilated

low alveolar ventilation (Va)

• lower pO2 no CO2 change

what happens to Va/ Q when

• overventilated

high alveolar ventilation (Va)

insufficient blood flow (Q)

consequences of high CO2

lowers pH of CSF and blood

detected by carotid/ aortic bodies

autonomic control centre in pons/ medulla

resp. motor neurones—> muscles

= increase rate and depth of breathing= remove more CO2

consequences of O2 treatment being too high

removes hypoxic drive

type 1 respiratory failure

low PaO2 AND low PaCO2

examples of type 1 respiratory failure

acute asthma

lung fibrosis

pulmonary embolism

type 2 respiratory failure

low PaO2 and HIGH paCO2

examples of type 2 respiratory failure

decreased ventilatory drive= sedative overdrive

decreased neuromuscular= myopathy

failure to reset chemoreceptors= COPD

what is asthma?

REVERSIBLE

chronic

bronchial hyperesponsiveness

= Bronchoconstriction

atopic triggers for asthma

Allergen- IgE

non-atopic triggers for asthma

exercise

chemicals

smoke

pathophysiological signs of asthma

smooth muscle cell spasm

bronchial inflammation

goblet cell hyperplasia

immune reaction to triggers in asthma

mast cells secrete histamine/ leukotrienes

infiltration of Th2 —> nitric oxides

chemokines —> damage and irritation to epithelium

diagnosis of asthma

spirometry

• Fev1/ FEC <0.7

asthma treatment

• relievers

short-acting beta-2-agonist: stimulate beta receptors to increase cAMP= bronchodilators e.g. Salbutamol

antimuscarinics: block ACh binding to muscarinic receptors

xanthine= relax smooth muscle/ bronchodilator

asthma treatment

• preventors

leukotriene receptor agonists= block leukotrienes causing bronchospasm

glucoticosteroid- synthesised from cholesterol to reduce pro-inflammatory mediators

monoclonal antibodies

long-acting Beta-2-adrenoreceptors- stimulate beta receptors to increase cAMP= bronchodilators e.g. Salmeterol

side effects of Beta-2-adrenoreceptors

muscle tremores

headaches

increased heart rate

hypokalaemia

side effects of glucoticosteroids

oral candidiasis- less T-cells

decreased bone density

adrenal supression

oral side effects of asthma/ COPD treatments

inhaler: dry mouth—> caries

bronchodilator: GERD

corticosteroids:oral candidiasis (reduced T-Cells)

what to do in dental setting if patient has Asthma

avoid triggers e.g. stress/ NO2

asthma pump and salbutamol available

avoid NSAIDS- inhibit COX1/2= less prostoglandins; more leukotrines= bronchospasm

• pulse ox. <95% = low flow 24-28% O2 (avoid removing hypoxic drive)

what can cause normal bronchocontriction of the lungs

parasympathetic innervation

ACh

Histamine

what causes natural bronchodilation of the lungs?

Sympathetic innervation

beta-2 receptor activation

whar is COPD?

chronic obstructive pulmonary disease

IRREVERSIBLE

chronic

restricted air flow affecting gas exchange

• chronic bronchitis

• emphysema

what is chronic bronchitis?

chronic airway inflammation

= affects expiration and inspiration

pathophysiological signs of chronic bronchitis

increased mucus

narrowed airway

fewer cilia

signs and symptoms of chronic bronchitis

• productive cough for 3 months within 2 years

• elevated haemoglobin

• oedema

• overweight

• cyanotic

what is emphysema?

enalrged alveoli

= affects expiration

pathophysiological signs of emphysema

• damaged epithelium= increased cytokines

• loss of elastase in alveolar connective tissue

• large air spaces

signs and symptoms of emphysema

• dyspnoea- increased CO2= barrel chested

• overinflated lungs= smaller heart, flattened diaphragm

• RHS heart failure

• thin

treatments for COPD

anticholinergics- block ACh at receptors= relax smooth muscle and decrease Mucus

Beta-2 adregenic Agonists- stimulate beta receptors to increase cAMP= bronchodilators

corticosteroids- inhibit immune response

cardiac cycle definition

series of electrical and mechanical events dictating blood flow through the heart to the circulation with each beat

role of pacemaker cells

set intrinsic heart rate

location of pacemaker cells

SA node in RA

AV node

purkinje fibres

how do pacemaker cells work?

unstable resting potential in heart

cells spontaneously depolarise

effect of parasmpathetic autonomic innervation to heart rate

open more K+ channels

• longer to reach resting potential

= slow HR

effect of sympathetic autonomic control on heart rate

open more Na+ channels

• shorter time to reach resting potential

= increases Heart rate

effect of adrenaline hormone on heart rate

increases heart rate

normal Heart rate

50-90 BPM

why do the pacemaker cells in SA node usually set the heart rate?

fastest depolarisation

cardiac cycle electrical pathway

1. SA node

2. internodal pathway

3. AV node

4. AV bundle

5. Bundle of His

6. Purkynje fibres

why is electrical conduction across AV node slower than across atria?

allows Atrial systole

how is ventricular myocardium specialised for rapid cell-cell conduction?

intercalated disks

gap junctions

how does ECG measure cardiac cycle

amalgamation of ion movements/ all action potentials in heart

what does P-wave on ECG show?

impulse travels from SA to AV node

atrial depolarisation

= ATRIAL SYSTOLE

what does QRS complex on ECG show?

impulse travels from AV node —> bundle of His —> Purkinje fibres

ventricular depolarisation

= VENTRICULAR SYSTOLE

(+ atrial repolarisation)

when does atrial repolarisation begin on ECG?

QRS complex

• but masked because more ventricular cells

what occurs during T-wave on ECG?

ventricular repolarisation

= ventricular and atrial DIASTOLE

how does blood move throughout the heart?

triggered by electrical events

pressure changes

what can be used to visualise the mechanical events of the cardiac cycle?

Wigger’s diagram

what valves are open in P-wave?

mitral valve open

• pressure in atria > ventricle

what valves are closed in P-wave?

Aortic valve

• pressure in ventricle < Aorta

what valves are open in QRS complex?

aortic valve open

• pressure in ventricle > aorta

what valves are closed in QRS complex?

mitral valve closed= LUB

• pressure in ventricle > atrium

what valves are open in T-wave?

mitral valve open

• pressure in atrium > ventricle

what valves are closed in T-wave?

aortic valve closed= DUB

• pressure in aorta > ventricle

what do the heart sounds represent?

LUB= mitral valve closing in ventricular systole

DUB= aortic valve closing in diastole

what causes systolic murmur?

• aortic valve not open

• mitral valve not closed

= extra sounds when LV contracting

what causes diastolic murmurs?

• mitral valve not closed

• aortic valve not open

= extra sounds when LV relaxed

stenosis vs regurgitation

narrowing= valve not opening

Leaking= valve not closed

autoimmune disease definition

specific immune responses to self-antigens resulting in pathology

what can non-organ specific autoimmune diseases affect?

DNA

Histones

IgG

what is involved in innate immunity

• macrophages; neutrophils- pattern recognition

• protective barriers

what is involved in Adaptive immunity?

• b-cells- recognise soluble antigens

• T-cells- recognise foreign molecules expressed by self-cells

what are 3 key characteristics of adaptive immunity?

• memory- cleared faster on reinfection

• specificity to single antigen

• discriminate between self (host) and non-self (foreign) cells

role of B-cells

bind to complementary antigens

clonal expansion into daughter cells that differentiate

• memory cells

• plasma cells- secrete antibodies

IgG

blood, tissue, placenta

• fix complement

• bind phagocytes

• neutralise toxins