Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 2 Biopharmacy > Bio > Flashcards

Bio Flashcards

1
Q

Gas exchange

A

ability of lungs to transfer air in and out effectively

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Ventilation

A

movement of air to alveoli providing O2 and removing CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Minute ventilation

A

amount of air exchanged per minute.

Tidal volume x respiratory rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Hypoxaemia

A

low levels of O2 in blood stream

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Hypercapnia

A

high levels of CO2. Occurs when person does not breathe out efficiently

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does V-Q mismatch stand for?

A

Ventilation-perfusion mismatch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the 2 circumstances known as V-Q mismatch?

A

1) Obstruction in air passages means air is unable to get to alveoli, so blood passing around those alveoli do not receive O2.
2) Conversely, areas of lungs where there are circulatory issues preventing blood flow can be well oxygenated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Perfusion

A

amount of blood flow to alveoli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Where in the lung is perfusion better?

A

at the base

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Pulmonary shunt

A

perfusion without ventilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Deadspace

A

ventilation that does not partake in gas exchange

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Atopic asthma

A

triggered by environment. Common. Inflammation caused by systemic IgE production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Non atopic asthma

A

Rare. Inflammation not caused by exposure to allergen. Inflammation caused by local IgE production.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Differences in bronchiole layers with asthma

A

more goblet cells, mast cells, T helper cells, neutrophils and larger smooth muscle cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

3 characteristics of asthma

A

airflow obstruction, bronchioles hyper responsive due to histamine release and inflammation due to increased neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does the body react to asthma - process

A

Inhale antigen, engulfed by dendritic cells which activates them. Columnar epithelial cells release thymic stromal lymphocytes which causes the dendritic cells to produce chemokines to attract T helper 2 cells to the lungs. These stimulate plasma cells and promote IgE production. These bind to mast cells to create a complex that the antigen will bind to, causing it to release histamine which causes constriction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Haldane effect

A

haemoglobin can hold either O2 or CO2, not both but will prioritise O2. If they can’t get rid of the CO2, they will take it back round. If given too much O2, will dump the CO2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

VQ mismatch when COPD patient given high flow oxygen

A

Chemoreceptors vasoconstrict areas that aren’t gas exchanging properly and move the blood elsewhere. When given high flow O2, chemoreceptors will open these vascular beds and allow blood to go to areas that still aren’t gas exchanging, so the blood will return to circulation full of CO2 and very little O2.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Pertussis

A

whooping cough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Hypersensitivity

A

altered immune response to an antigen that causes the person to become ill.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Autoimmunity

A

body creates antibodies to fight own cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

alloimmunity

A

body creates antibodies to fight foreign antigen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

4 types of hypersensitivity reactions

A

1) IgE reaction
2) Tissue specific reaction
3) Immune complex mediated reactions
4) Cell-mediated reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Innate immunity

A

1st line of defense. Phagocytes, dendritic, mast, complement, mediators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Adaptive immunity

A

2nd line of defence. B, T killer and helper cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Biochemical mediators and their functions

A

histamine - redness
bradykinin - pain
leukotrienes and prostaglandin - vasodilation

they all cause the cells of the vessel endothelial lining lining to retract so leukocytes and plasma enter the surrounding tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

IgG

A

antiviral, antibacterial and antitoxin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

IgA

A

in saliva, tears and colostrum. Acts locally on mucosa in respective tissues, preventing viruses from attaching to epithelium.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

IgM

A

largest. Helps digest and eliminate organisms. Found in foetus.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

IgE

A

allergic reactions and parasites.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What does an antibody link to?

A

cell membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are some pleural membrane issues?

A

fluid can accumulate between layers of lung, in intrapleural space or there can be a hole within pleura, so lung can’t be pulled out easily.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Visceral pleura

A

adheres to lungs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Parietal pleura

A

sac where lung sits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Functions of pleura

A

allows lung to change shape and prevents it collapsing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Pleuritis

A

inflammation of parietal pleura. Shows as shortness of breath, chest pain and pleural rub

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Pleural effusion

A

accumulation of fluid in pleural space, usually as result of inflammation of pleura. Less breath sounds and decreased lung expansion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Pneumothorax

A 
accumulation of air in pleural space.
1) spontaneous - ruptured bullae
2) open - external trauma
Causes lung to collapse
will be no breath sounds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Tension pneumothorax

A

overaccumulation of air in pleural space, usually as result of valve mechanism. air enters during inhalation but then cannot leave, increase in pressure causes lung to skip. LIFE THREATENING

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Pneumonia

A

lung inflammation caused by infection. affects lower airway and causes development of secretions which build up and block airways, causing lung collapse.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Causative agents of pneumonia

A

Bacteria - strep, haemophilus influenza, legionella, staph, mycoplasma

Virus - influenza, RSV

Fungi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How does body react to bacterial pneumonia?

A

Bacteria enters alveoli; macrophages produces cytokines. These cause vasodilation and increased vascular permeability - causes fluid to shift from vascular space to alveoli, leading to congestion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How does body react to viral pneumonia?

A

Virus infects respiratory cell and releases genetic material. Uses hosts proteins to replicate - damages cell, creating cell debris, initiating immune response. macrophages produces cytokines. These cause vasodilation and increased vascular permeability - causes fluid to shift from vascular space to alveoli, leading to congestion.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

How does body react to fungal pneumonia?

A

Fungi spores inhaled - travels to alveoli where it grows into fungal ball. Can spread, causing systemic effect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Effects of lung infection

A

fluid filled alveoli, increased mucus secretion, narrowed airways and bronchi constriction.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Consolidation

A

the process that fills the alveoli with fluid, pus, blood and cells resulting in lower diffuse capacity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

lobar pneumonia

A

affects whole lobe. 4 stages:

1) congestion
2) red hepatization
3) grey hepatization
4) resolution

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Broncho pneumonia

A

starts with bronchioles, moves to alveoli. affects patches.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Tool used to assess severity of pneumonia

A

CURB-65. Score greater than 2 = hospitalisation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Transmission of pneumonia

A
  • inhalation of infected agents
  • aspiration of organisms that colonize oropharynx
  • aspiration of stomach content
  • haematological spread
  • direct innoculation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

complications of pneumonia

A

abscess, empyema, bacteremic dissemination

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Empyema

A

pockets of pus that have collected inside a body cavity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

4 investigations for pneumonia

A

chest xray, sputum testing, urine antigen testing, blood testing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Management and treatment of pneumonia

A

O2, IV fluids, pain management, antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Stridor

A

harsh noise on inspiration due to narrowing of larynx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Rhonchi

A

low pitched, gurgling noises with severe infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Grunting

A

typical in babies when they trap air in lower airway by prematurely closing off glottis at end of breath.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Bronchospasm

A

bronchi spasm and constrict, narrowing airway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Laryngospasm

A

narrowing of larynx. Can fully close airway and prevent breathing.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Apnoea

A

absence of breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

dyspnoea

A

difficulty breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Tachypnoea

A

fast breathing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Crackles

A

sound made when secretions not fully cleared by coughing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Cor pulmonale

A

abnormal enlargement of right side of heart due to disease in lungs and/or pulmonary blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Epistaxis

A

nose bleed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Haemoptysis

A

coughing up blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Hypoxaemia

A

low concentration of oxygen in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Hypoxia

A

part of body deprived of oxygen at tissue level

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

What happens to foetal circulation after birth?

A

systemic vascular resistance rises.
alveoli expands and vessels around them dilate.
Pulmonary pressure decrease. 6-8 wks before pulmonary vascular resistance is normal.
Increase in left atrial pressure (blood returns to heart from pulmonary tissue) forces septum primum against septum acundum, closing foramen ovale.
Ductus arteriosus and ductus venosus close (leaves ligamentum venosum)
Umbilical vein and arteries are infiltrated with fibrin and also become ligaments.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Transporter carriers

A

carry single molecule in one direction across membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Symporter carriers

A

carry two molecules in same direction across membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Antiporter carriers

A

carry two molecules in different directions across membrane

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Pharmacodynamics

A

what drug does to body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Pharmacokinetics

A

what body does to drug

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

4 kinds of protein drug targets

A

enzymes, carrier/transporter, ion channels, receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

How does drug work with ion channels?

A

drug facilitates opening or blocking of channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

How does drug work with enzyme?

A

drug inhibits enzymes by binding to it

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

How does drug work with carrier/transporter?

A

drugs inhibit or facilitate transport of molecules that use carriers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

How does drug work with receptor?

A

drug will bind to receptor and either mimic or block body’s own natural chemical signals

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Agonist

A

drugs that mimics body’s signal, enhances effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Antagonist

A

drugs that block body’s signal, blocking effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Two components of drug-receptor interactions

A

Binding of drug to receptor, governed by affinity

Activation of response, governed by efficacy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Drug potency

A

combination of affinity and efficacy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Competitive antagonist

A

competes with agonist/body’s signal for receptor binding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Irreversible antagonist

A

dissociates from receptor very slowly or not at all, so no change occurs when additional agonist added

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

non competitive antagonist

A

does not affect agonist binding, instead interrupts chain of events after

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

chemical antagonism

A

antagonist combines with drug in solution such that the effect of the active drug is lost

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Pharmacokinetic antagonism

A

VERY COMMON. Antagonist reduces concentration of another drug by altering how it is passed through the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Physiological antagonism

A

antagonist has opposing biological action of agonist so tends to cancel action out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

4 main stages of pharmacokinetics

A

absorption, distribution, metabolism and excretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What are the 4 ways that drugs can cross membranes?

A
  • diffusion through lipid
  • diffusion through aqueous membrane
  • combination with carrier molecule
  • pinocytosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Where is carrier mediated drug transport important?

A

renal tubule, biliary tract, blood-brain barrier and GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Bioavailability

A

proportion of drug that reaches circulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Where does absorption of drugs mainly occur and why?

A

in the small intestine because of the large absorptive surface area of the villi and microvilli of the ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Why does pH matter in drug absorption?

A

it makes drugs more/less lipid soluble

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Factors affecting drug absorption

A 
rate of gastric emptying
disease
transit time through gut
blood flow
age
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Plasma-protein drug binding

A

some drugs exist in plasma bound to plasma proteins, but only the free, unbound drug can exert a pharmacological effect

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Factors that affect drug distribution

A 
adiposity
plasma protein concentration
blood flow
membrane permeability
body water content
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

hypertonic

A

higher concentration of solute than water

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

hypotonic

A

higher concentration of water than anything else

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Carcinogen

A

a substance or situation that results in cancer developing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Carcinoma

A

arises from epithelial tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

Leukaemia

A

tumour that starts in blood-forming cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

Lymphoma

A

tumour that starts in lymphatic tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Metastases

A

spread of cancer cells from the site of the original tumour to elsewhere in the body. Different cancers have different patterns of spread.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Neoplasm

A

abnormal mass of cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Sarcoma

A

tumour starting in connective tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

Tumour

A

an abnormal growth resulting from uncontrolled proliferation of cells. It serves no physiological function for the person.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

Benign tumour

A

grows slowly, well defined capsule, not invasive, look like the tissue where they occur, don’t metastasize

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

Malignant tumour

A

grows rapidly, not encapsulated, invade local structures and tissues, poorly differentiated, may not be able to determine the tissue of origin, spread to distant areas of the body (via blood and lymph). Cells in a malignant tumour typically have an irregular sized and shaped nucleus with a loss of normal tissue structure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Autonomy

A

cell that works independently from other cells (as a cancer cell)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Angiogenesis

A

development of new blood vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Apoptosis

A

programmed cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Chemotherapy

A

encompass medications that can affect the vulnerability in the cell wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Epigenetics

A

involves the change in gene coding which doesn’t change DNA sequencing but ‘switches’ genes on or off, often in the expression of RNA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Oncogene

A

a gene that in its normal state (as a proto-oncogene) makes (synthesises) proteins to support the replication of cells. Once it mutates into an oncogene, it supports the replication of cancer cells.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Silencing

A

chemical changes can silence a gene, without it mutating. Silencing a tumour suppressing gene can mean a cancer then develops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Tumour marker

A

substance produced by a tumour cell which is either present on the tumour cell or in blood, spinal fluid or urine, eg Prostate Specific antigen (PSA)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

What happens during deep wound healing?

A

blood clot forms during inflammatory response - loosely unites the wound edges.

Migratory phase - clot becomes scab + epithelial cells migrate beneath to bridge wound. Fibroblasts begin synthesizing scar tissue and damaged blood vessels begin to regrow. The tissue filling the wound is called granulation tissue.

Proliferative phase - growth of epithelial cells, deposition of collagen fibres and continued growth of blood vessels.

Maturation - scab sloughs off once the epidermis has been restored to normal thickness. Collagen fibres become more organized, fibroblasts decrease in number and blood vessels are restored to normal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Primary Dysmenorrhoea

A

painful menstruation which occurs with the release of a substance called prostaglandin, which constricts blood vessels and stimulates the uterine muscle to contract, increasing the sensitivity of the nerves to pain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Primary Amenorrhoea

A

lack of menstruation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Polycystic ovaries

A

a disease where instead of follicles developing and releasing each month, cysts develop within the ovary.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Salpingitis

A

a commonly seen condition where the uterine (fallopian) tubes become inflamed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Oophoritis

A

inflamed ovaries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Prolapse

A

pushing of one organ into another

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Endometriosis

A

uterine tissue that is out of place

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

Galactorrhoea

A

the excess secretion of milky substances from the nipple when the woman is not breast-feeding or pregnant.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
128
Q

Gynecomastia

A

overdevelopment of breast tissue in men.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
129
Q

Cryptorchidism

A

where the testes don’t descend fully in the first few months after birth and stops in the abdomen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
130
Q

Orchitis

A

infection of testes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
131
Q

Benign prostatic hyperplasia

A

an enlarged prostate gland which can compress the urethra giving urinary problems.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
132
Q

Serum osmolality

A

concentration of ions in blood plasma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
133
Q

Acute renal failure definition

A

reversible decrease in glomerular filtration rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
134
Q

What are the signs of acute renal failure?

A

decreased glomerular filtration rate
sudden increase in creatinine level
decreased urine output

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
135
Q

Pre renal causes of ARF

A

sudden increase in BP or flow obstruction in kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
136
Q

Intra renal causes of ARF

A 
direct damage to kidneys
inflammation
infection
drugs
autoimmune disease
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
137
Q

Post renal causes of ARF

A

obstruction of urine flow (kidney stones, bladder injury, tumour etc.)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
138
Q

4 types of intrarenal failure

A
  • acute glomerular nephritis
  • acute tubular necrosis
  • acute interstitial nephritis
  • vascular
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
139
Q

Two changes that cause a decrease in glomerular filtration rate

A

vascular or tubular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
140
Q

Atrophy

A

decrease in cell size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
141
Q

Hypertrophy

A

increase in cell size

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
142
Q

Metaplasia

A

reversible change where one adult cell is replaced by another type of adult cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
143
Q

Dysplasia

A

irregular set of cells that develop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
144
Q

Apoptosis

A

pre programmed cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
145
Q

Haematopoiesis

A

formation of blood cellular components

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
146
Q

neutrophils

A

first at site of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
147
Q

basophils

A

allergy and parasitic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
148
Q

eosinophils

A

allergy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
149
Q

monocytes

A

circulating macrophages - turn into macrophages or dendritic cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
150
Q

megakaryocytes

A

release platelets for clotting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
151
Q

Angiogenesis

A

new vessel formation and maturation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
152
Q

Acute leukaemia

A

comes from most acute cells (blasts).
Acute lymphoblastic leukaemia - B cell and T cell
acute myeloid leukaemia - myelo, mono and megakaryo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
153
Q

Chronic leukaemia

A

Chronic lymphoid leukaemia comes from B cells - travel to lymphnode, spleen and liver, which all enlarge. L.N creates generalised lymphnode nopathy, leading to a small lymphocytic lymphoma. This can create a diffuse B cell lymphoma.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
154
Q

Sickle cell anemia

A

genetic disease where red blood cells take the shape of a sickle, allowing them to be more easily destroyed.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
155
Q

Vaso occlusion

A

sickle red blood cells get stuck in capillaries. This can clog up bones, leading to a wide number of issues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
156
Q

Effect of repeated sickling

A

damages cell membrane, causing haemoglobin to spill out. This is recycled by haptoglobin which lead to unconjugated bilirubin - causing scleral icterus, jaundice and bilirubin gallstones.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
157
Q

Extra treatment for sickle cell anemia in children

A

prophylaxis, penicillin and polysaccharide vaccine. Prevents sepsis and meningitis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
158
Q

Primary intention

A

wound is clean, little/no tissue loss. Tissue edges brought together with stitches, staples etc.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
159
Q

Secondary intention

A

wound edges cannot be brought together because of extensive tissue loss.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
160
Q

Tertiary intention

A

would edges could be brought together but not done immediately due to contamination or infection.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
161
Q

hypertrophies

A

abnormal enlargement of a part or organ; excessive growth

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
162
Q

What medication is used in asthma as an anti-inflammatory to reduce the level of inflammation?

A

corticosteroid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
163
Q

What does the MHC or HLA system do?

A

triggers the changing of monocytes into macrophages to engulf invading organisms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
164
Q

Which of the tissue mediators creates the feeling of pain?

A

Bradykinin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
165
Q

Which organs are involved in the development and storage of T and B lymphocytes?

A

thymus, kidney and liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
166
Q

Which receptors sense a change in the concentration of dissolved particles in the blood stream?

A

osmoreceptors in the hypothalamus detecting osmolarity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
167
Q

Diabetes insipidus

A

not enough ADH is produced which means the kidney cannot make enough concentrated urine and too much water is passed from the body.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
168
Q

The force of the hydrostatic pressure is produced by?

A

blood pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
169
Q

proto-oncogenes

A

normal genes that help cells grow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
170
Q

oncogene

A

cancer causing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
171
Q

tumour suppressor genes

A

encode for proteins that are involved in inhibiting the proliferation of cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
172
Q

stages of carcinogenesis

A

initiation, promotion and progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
173
Q

carcinoma

A

Epithelial cell cancer

174
Q

sarcoma

A

cancer in supportive and connective tissue cells

175
Q

lymphoma

A

cancer in glands or nodes in the lymph system

176
Q

myeloma

A

cancer in plasma cells in the bone marrow

177
Q

leukaemia

A

blood cell cancer

178
Q

Which processes occur within the S-phase of the cell cycle?

A

replication of DNA and centrosomes

179
Q

What is the rule of 9s?

A

Used in burns, the entire surface of the human body is divided into 11 areas, with each given a value of 9%. This adds up to 99% of the surface of the body, with the groin being the final 1%.

180
Q

What is endometriosis?

A

a condition where tissue similar to the lining of the womb starts to grow in other places, such as the ovaries and fallopian tubes.

181
Q

In premenstrual tension, hormonal levels can change quickly resulting in mood changes, depression, irritability and aggression.
What substances in the body are most likely to be linked to these symptoms developing?

A

Neurotransmitters eg serotonin

182
Q

What is oophoritis?

A

inflammation of ovaries

183
Q

What is prolapse?

A

when 1 or more of the organs in the pelvis slip down from their normal position and bulge into the vagina.

184
Q

balanitis

A

infection of male glans

185
Q

cryptprchidism

A

undescended testes

186
Q

Difference between adult and foetal haemoglobin

A

Foetal haemoglobin has a higher affinity for oxygen so sats might be lower

187
Q

Signs of cancer - CHILDREN

A 
C - continuous unexplained weight loss/fatigue
H - headaches with vomiting
I - increased oedema or pain
L - lump or mass
D - development of whiteness in pupil of eye
R - recurrent or persistant fevers
E - excessive bruising/bleeding
N - noticeable pallor/anaemia
188
Q

treatments for cancer

A

chemotherapy, surgery, radiation, stem cell transplantation, steroid therapy, biological agents

189
Q

How many cells thick is a normal alveolus?

A

1

190
Q

FEV1

A

measure of air flow rate through the lungs

191
Q

What medication is used in asthma as an anti-inflammatory to reduce the level so inflammation?

A

corticosteroid

192
Q

How could obesity affect excretion of drugs?

A

Increased BP and impaired renal function

193
Q

What would be a normal value for intracranial pressure?

A

0-15 mmHg

194
Q

If eyes are different sizes, which nerve is being affected?

A

oculomotor

195
Q

Which sympathetic response is mismatched with its body part?

A

stomach - decreased mobility

196
Q

Which structure would the medulla oblongata potentially move through to cause brain stem death?

A

foramen magnum

197
Q

What is the sequence of the vertebrae, starting at the head and moving down the body?

A

cervical, thoracic, lumbar, sacral, coccyx

198
Q

What is the name given to the first cervical vertebra on which the skull is attached?

A

atlas

199
Q

How could obesity affect absorption of IM/SC drugs?

A

thick layer of adipose tissue with impaired blood flow to peripheries

200
Q

Allodynia

A

pain resulting from a stimulus (such as light touch) that does not normally elicit pain.

201
Q

If eyes are different sizes, which nerve is likely to be being compressed?

A

Cranial nerve 3 - oculomotor

202
Q

How could obesity affect excretion of drugs?

A

Increased BP and impaired renal function

203
Q

What is FEV1?

A

measure of air flow rate through lungs

204
Q

Which organelle within the cell changes the proinsulin to insulin and also produces a molecule of c-peptide?

A

ribosomes on ER

205
Q

Hypoalgesia

A

diminished response to normally painful stimuli.

206
Q

Hyperesthesia

A

increased sensitivity to stimulation.

207
Q

Hypesthesia

A

diminished sensitivity to stimulation.

208
Q

ventricular fibrillation

A

A serious heart rhythm problem in which the heart beats quickly and out of rhythm. No clear waves

209
Q

Paresthesia

A

an abnormal sensation, spontaneous, or evoked.

210
Q

Allodynia

A

pain resulting from a stimulus (such as light touch) that does not normally elicit pain.

211
Q

If eyes are different sizes, which nerve is likely to be being compressed?

A

Cranial nerve 3 - oculomotor

212
Q

What is FVC?

A

forced vital capacity - determines the amount of air that can be forcibly exhaled

213
Q

What is FEV1?

A

forced expiratory volume - amount of air you can force from your lungs in one second

214
Q

Tidal volume

A

the volume of air moved between one normal inhalation and one normal exhalation.

215
Q

Inspiratory reserve volume

A

The amount of extra air inhaled — above tidal volume — during a forceful breath in.

216
Q

Which are more potent: agonists or antagonists?

A

agonists

217
Q

ventricular fibrillation

A

A serious heart rhythm problem in which the heart beats quickly and out of rhythm. No clear waves

218
Q

What medication can be used to treat hypertension?

A

diuretics

219
Q

What can cause plaque formation in brain?

A

Abnormal enzymic breakdown of B-amyloid associated protein

220
Q

glucose and water equation

A

C6H12O6 + 6O2 ↔ 6CO2 + 6H20

221
Q

gluconeogenesis

A

breaking down fats

222
Q

glucogenolysis

A

breakdown of glycogen to glucose-1-phosphate and glycogen.

223
Q

effect of insulin on gluconeogenesis and glycogenolysis

A

decreases both

224
Q

What check occurs in G2 of cell cycle?

A

The cell checks for any incomplete replication of the DNA prior to mitosis

225
Q

5 stages of embryonic lung development

A

Day 22 - buds appear from primitive oesophagus
Embryonic (4-7wks) - lung bud, trachea and bronchi, pulmonary vein and artery
Pseudoglandular (7-17wks) - conducting airways, terminal bronchioles
Canalicular (17-26wks) - primitive alveoli, type l and ll cells, surfactant synthesis
Saccular (27-36wks) - alveolar saccules, extracellular matrix, neural network maturation
Alveolar (36wks - 2yrs) - expansion of gas exchange area, nerves and capillaries

226
Q

Embryological lung issues

A

failure of oesophagus to form as lung buds create a blind pouch, resulting in oesophagus atresia.
Can be connected to trachea causing tracheal-oesophageal fistula

227
Q

role of osteoblasts

A

build bone

228
Q

role of osteoclasts

A

break down bone

229
Q

what are osteocytes?

A

mature bone cell

230
Q

What happens during G1 of cell cycle?

A

duplicates organelles and cytosolic components. Checks DNA for damage, if its growing enough and that it has enough resources

231
Q

what is an osteon?

A

functional unit of compact bone

232
Q

difference in children’s airway anatomy

A

large tongue and tonsils, floppy epiglottis, short trachea, narrow airways, higher larynx, respiratory muscles developing

233
Q

How do we stage tumours? 3 factors

A

Tumour - size, location, local extent
Node - spread?
M - metastatic

234
Q

5 stages of embryonic lung development

A

Embryonic (4-7wks) - lung bud, trachea and bronchi, pulmonary vein and artery
Pseudoglandular (7-17wks) - conducting airways, terminal bronchioles
Canalicular (17-26wks) - primitive alveoli, type l and ll cells, surfactant synthesis
Saccular (27-36wks) - alveola saccules, extracellular matrix, neural network maturation
Alveolar (36wks - 2yrs) - expansion of gas exchange area, nerves and capillaries

235
Q

Embryological lung issues

A

failure of oesophagus to form as lung buds create a blind pouch, resulting in oesophagus atresia.
Can be connected to trachea causing tracheal-oesophageal fistula

236
Q

coanal atresia

A

congenital disorder where the back of the nasal passage is blocked, usually by abnormal bony or soft tissue due to failed recanalization of the nasal fossae during fetal development.

237
Q

cystic fibrosis

A

defect on single chromosome 7q31.2 - should code for regulator which controls passage of chloride across cell membrane. In CF, ability to reabsorb sodium and chloride is lost, so sweat is salty, secretions are thick and hard to expel

238
Q

In which part of the cell cycle do cells exit?

A

G0

239
Q

What happens during G1 of cell cycle?

A

duplicates organelles and cytosolic components. Checks DNA for damage, if its growing enough and that it has enough resources

240
Q

What check occurs during the mitotic phase?

A

are the chromosomes lined up correctly?

241
Q

senescence

A

loss of a cell’s power of division and growth.

242
Q

How do we stage tumours? 3 factors

A

Tumour - size, location, local extent
Node - spread?
M - metastatic

243
Q

How does oedema occur?

A

when small blood vessels leak and release fluid into nearby tissues which builds up and causes swelling

244
Q

Wilm’s tumour

A

kidney tumour.

composed of 3 cellular types: stromal, epithelial and blastemic.

245
Q

blastemic cells

A

undifferentiated, may have partly changed into stromal or epithelial

246
Q

2 types of wilms tumours

A

sporadic - no known genetic issues

inherited - rare but can be inherited in autosomal dominant fashion

247
Q

genetic abnormalities associated with wilms tumour

A

aniridia - loss of iris
hemihypertrophy - body asymmetry
hypospadias - opening of penis underneath rather than tip
genitourinary malformations

248
Q

Remission and maintenance phase of leukaemia chemo

A

2-3yrs

Drugs: methotrexate, vincristine, dexamethasone, mercaptopurine

249
Q

How can chemo meds work?

A
  • inhibit synthesis of nucleotides in DNA +/or RNA
  • altering base pairing of DNA/RNA
  • inhibiting enzymes
  • directly affecting DNA
250
Q

alkylating agents

A

form covalent bonds with DNA and stop replication

251
Q

antimetabolites

A

block one or more metabolic pathways

252
Q

cytotoxic antibiotics

A

prevent cell division

253
Q

plant derivatives in chemo

A

affect how spindle forms in mitosis

254
Q

Induction phase of leukaemia chemo

A

4-6wks
Obj: eradicate 99% of leukaemic blasts
Drugs used: dexamethasone, vincristine, asparaginase, daunorubicin

255
Q

Consolidation phase of leukaemia chemo

A

4-12wks
Obj: eradicate residual leukaemic blasts and reduce risk of bone marrow and CNS relapse
Drugs: vincristine, dexamethasone, thiopurine, methotrexate

256
Q

Delayed intensification phase of leukaemia chemo

A

8-12wks
Obj: reduces relapse risk
Drugs: methotrexate, vincristine, dexamethasone, doxorubicin, asparaginase, cyclophosphamide, cytarabine, thioguanine

257
Q

Remission and maintenance phase of leukaemia chemo

A

2-3yrs

Drugs: methotrexate, vincristine, dexamethasone, mercaptopurine

258
Q

graft vs host disease

A

cells from body and transplant can attack each other - would have to take immunosuppressants for life

259
Q

astrocytomas - where and what from?

A

found throughout brain, slow growing.
arise from glial astrocyte cells.
Cerebellar or supratentorial

260
Q

medullablastoma - what from and movement?

A

arise from primitive neuro-epithelial cells

metastases along CSF pathway

261
Q

craniopharyngioma - where and what from?

A

midline tumour usually around pituitary gland

formed from epithelial cells and cysts

262
Q

brain stem tumours - what do they start from?

A

arise from primitive glial cells

263
Q

Digestive system blood supply

A

delivered via mesentric artery but returned by hepatic portal vein into liver rather than general circulation. This is so sugars can be stored in liver as glycogen.

264
Q

Where does most dug metabolism occur?

A

liver

265
Q

Where are cytochrome P450 enzymes kept?

A

smooth ER

266
Q

What do cytochrome P450 enzymes do?

A

metabolise unwanted substances into a from easier to excrete in urine

267
Q

foods that are CYP450 inhibitors

A

grapefruit + cranberry juice, watercress, gingko bilboa, ginseng

268
Q

Phase ll reactions

A

attach molecule to the unwanted substance, making it more water soluble and easier for kidneys to excrete

269
Q

enterohepatic recirculation

A

bile salts are recycled so some drugs can reappear in circulation along with bile, giving them a longer half life (e.g. morphine and rifampicin)

270
Q

4 ways that drugs can cause side effects

A

1) tipping balance too far
2) hitting unwanted target - might hit receptors causing another effect e.g. salbutamol binds to receptor in heart causing tachycardia
3) autoimmune reactions
4) drugs that are intrinsically hazardous - some drugs work by inflicting damage on rapidly dividing cells so may affect healthy cells

271
Q

Therapeutic index

A

minimum effect concentration / maximum safe concentration

272
Q

effect of immature liver on drugs metabolism

A

metabolises faster so cannot generalise rate of drug metabolism in younger children

273
Q

Which drug is prescribed based on race?

A

ACE inhibitors

274
Q

metabolism definition

A

conversion of one chemical entity to another

275
Q

foods that are CYP450 inducers

A

leafy greens, cigarettes, alcohol, st johns wart, valerian, gingko bilboa

276
Q

foods that are CYP450 inhibitors

A

grapefruit + cranberry juice, watercress, gingko bilboa, ginseng

277
Q

Who is at greatest risk following paracetamol overdose?

A

those with liver damage

278
Q

factors affecting metabolism

A

age - reduced first pass metabolism, reduced hepatocytes and enzymes
disease - liver disease means reduced hepatocytes, reduced hepatic blood flow

279
Q

glomerular filtration in excretion

A

glomerular capillaries allow drugs to diffuse into glomerular filtrate unless too big or if they are bound

280
Q

diffusion across renal tubule - drug excretion

A

as filtrate transverses tubule, water is reabsorbed.

Lipophilic drugs are readily reabsorbed so excreted slowly. Highly polar drugs remain in tubule

281
Q

active tubular secretion - drug excretion

A

drug molecules transferred to the tubular lumen by two independent, non selective carrier systems. carriers can reduce plasma concentration of some drugs to almost 0.

282
Q

extrinsic receptors

A

outside circulatory system and respond more to environmental changes

283
Q

factors affecting excretion of drugs

A

disease - reduced renal blood flow

age - renal function reduced as you get older

284
Q

how does sympathetic system raise HR?

A

stimulates adrenergic receptors

285
Q

how does parasympathetic system lower HR?

A

via vagus nerve

286
Q

how do heart contractions occur?

A

SA node releases signals - sent to ventricles via AV node. AV node delays impulses on way to ventricles so sequence can occur in stages and peak cardiac output can be achieved. From AV node, impulse travels down bundle of His, separating into 2 branches towards ventricles. Faster down left - diff in speed allows them to contract together due to thicker myocardium around left ventricle. Branches end in purkinje fibres + then myocytes contract causing ventricular contraction.

287
Q

pulse pressure

A

difference between systolic and diastolic BPs

288
Q

mean arterial pressure definition

A

average pressure in arterial system during ventricular contraction and relaxation

289
Q

Mean arterial pressure calculation (MAP)

A

MAP = cardiac output (CO) x peripheral vascular resistance (PVR)

290
Q

Cushing’s triad

A

late sign of raised ICP:

  • decreased HR
  • increased BP
  • reduced RR and change in pattern
291
Q

extrinsic receptors

A

outside circulatory system and respond more to environmental changes

292
Q

effect of different hormones on BP

A

ADH - increases BP via vasoconstriction
Renin - increases BP by converting angiotensin
Angiotensin ll - increases BP via vasoconstriction, aldosterone release
Aldosterone - increases BP by increasing retention of sodium and water in kidneys

293
Q

list some common congenital heart defects

A

patent ductus arteriosus
patent foramen ovale
fallot’s tetralogy - combo of 4 defects
atrioventricular septal defect

294
Q

5 types of intracranial haemmorhage

A 
subdural - below dura mater
epidural - between skull and dural membrane
subarachnoid - within subarachnoid space
intracerebral 
intraventricular
295
Q

hydrocephalus

A

excessive accumulation of CSF in brain due to overproduction, flow obstruction or decreased absorption.

296
Q

Layers of skull

A
  • scalp
  • bone
  • dura mater
  • arachnoid mater
  • subarachnoid space
  • pia mater
  • brain tissue
297
Q

basic flow of CSF

A

produced by choroid plexuses
flows through ventricles into subarachnoid space
absorbed into dural venous sinuses via arachnoid villi

298
Q

management of hydrocephalus

A

shunt

control of cardiovascular events

299
Q

Cushing’s triad

A

late sign of raised ICP:

  • decreased HR
  • increased BP
  • reduced RR and change in pattern
300
Q

brain herniation

A

brain moves outside of skull or across into a structure within the skull

301
Q

supratentorial herniation

A

displacement of cerebrum

302
Q

infratentorial herniation

A

displacement of cerebellum

303
Q

focal mass effect of brain herniation

A

intracranial bleeds
tumours and abcesses
local oedema

304
Q

diffuse mass effect of brain herniation

A 
generalised cerebral oedema
cytogenic oedema - within cells
vasogenic oedema
large ischaemic stroke
meningitis
305
Q

uncal herniation

A

uncus slips down, puts pressure on brain stem and oculomotor nerve. Compresses cerebral artery. affects L/R vision, not central.

306
Q

3 main types of spina bifida

A

myelomeningocele - spinal cord and meninges protrude out of opening in bony vertebrae. Held by sac of skin that pouches out from back. Some have no skin, leaving spine exposed (paralysis).

meningocele - only in meninges - slip into gaps between deformed vertebrae. least common and less symptoms.

spina bifida occulta - most common. tiny deformities, asymptomatic.

307
Q

cingulate herniation

A

cingulate durus squeezed to opposite part of skull

308
Q

transcalvarial herniation

A

brain squeezes out of skull through fracture or surgical site

309
Q

upward herniation

A

cerebellum displaced upwards

310
Q

tonsilar herniation

A

cerebral tonsils slip down through foramen magnum

CONING

311
Q

classification of cerebral palsy

A

spastic - tight/stiff muscles, jerky, hypertonia
dyskinetic - damage to basal ganglia. dystonia (random slow, uncontrolled movements in limbs or trunk) and chorea ( random dance like movements)
ataxic - damage to cerebellum. without order, poor balance and shaky

312
Q

what is cerebral palsy?

A

damage to brain causing paralysis

313
Q

what is spina bifida?

A

tissues on spinal cord don’t meet, leaving openings of unprotected spine

314
Q

how does spinal cord develop?

A

ectoderm develops ridge which becomes the neural tube. This becomes the spinal cord, brain and meninges.

315
Q

Two types of ADHD and how it is diagnosed?

A

1) inattentive - 9 symptoms
2) hyperactive - 9 symptoms
3) both

diagnosed if have 6/9 symptoms for at least 6 months

316
Q

what causes epilepsy?

A

neurons are synchronously active.

317
Q

what happens during seizure?

A

cluster of neurons sends out cluster of signals - too much excitation due to glutamate or too little inhibition due to gaba.

318
Q

what is cerebral perfusion pressure and how to calculate?

A

pressure required to maintain adequate cerebral blood flow:

CPP = MAP - ICP

319
Q

how to diagnose epilepsy?

A

brain imaging

electroencephalogram

320
Q

acceptable cerebral perfusion pressure (CPP)?

A

above 50-70mmHG

321
Q

role of glutamate

A

neurotransmitter which opens calcium ion channels (excites AP)

322
Q

role of gaba

A

neurotransmitter which opens chloride ion channels (this inhibits AP as makes the cell negative)

323
Q

Two types of ADHD and how it is diagnosed?

A

1) inattentive - 9 symptoms
2) hyperactive - 9 symptoms
3) both

diagnosed if have 6/9 symptoms for at least 6 months

324
Q

how many vertebrae are there and what are they?

A

33:

  • 7 cervical
  • 12 thoracic
  • 5 lumbar
  • 5 sacral
  • 4/5 occygeal
325
Q

slipped disc

A

cartilagenous tissue between vertebrae has bulged out

326
Q

hyperflexion of spine

A

when the spine is bent forwards exceeding the span of movement that is possible

327
Q

hyperextension of spine

A

when the spine is extended backwards, eg hit in the jaw and the head is forced backwards

328
Q

Axial injury of spine

A

when the person lands on their head or their feet and the force on landing travels upwards through the body and the spine, eg diving into swimming pools, catapulted over a car

329
Q

Rotation injury of spine

A

when the body twists as the person lands

330
Q

spinal dislocation

A

when ligaments are over-stretched or torn, which allows the spine to move out of line or vertebrae to ‘lock’ over each other.

331
Q

simple fracture

A

where the fracture leaves the vertebra in place, aligned with the other vertebrae and there are no neurological deficits.

332
Q

compression fracture

A

where the fracture is caused by an axial injury and hyperflexion

333
Q

wedge compression fracture

A

a stable fracture but also includes compression of the vertebra, typically this occurs in the neck area

334
Q

teardrop fracture

A

where a piece of the vertebra breaks away, making the fracture unstable

335
Q

comminuted fracture

A

where the vertebra shatters into small pieces. This is very unstable and will affect the spinal cord

336
Q

partial spinal cord syndrome

A

injury to one side of cord , leading o loss of movement of that side of body. Opposite side loses ability to maintain temp, sense pain and touch

337
Q

spinal shock

A

complete loss of function below level of spinal cord injury. communication between brain and bottom of spinal cord is disrupted.

338
Q

neurogenic shock

A

severe form of spinal shock, where sympathetic impulses to heart are lost

339
Q

quadriplegia

A

loss of leg function and partial/total loss of arm function

340
Q

paraplegia

A

loss of leg function

341
Q

hermiplegia

A

paralysis of one side of body

342
Q

posterior cord syndrome

A

some sensory +/or motor function is maintained

343
Q

anterior cord syndrome

A

some loss of motor function below injury

344
Q

factors affecting excretion in children

A

reduced GFR, reduced tubular secretion

345
Q

scoliosis

A

C or S shaped curved spine

346
Q

kyphorosis

A

exaggerated, abnormally round upper back

347
Q

lordosis

A

sway back, spine curves in more than normal at lower back

348
Q

when does spina bifida usually form?

A

day 22 when neural tube closes at each end

349
Q

factors affecting absorption in children

A

higher gastric pH in neonates, skin less developed so greater surface area, delayed gastric emptying, reflux, reduced muscle blood flow

350
Q

factors affecting distribution in children

A

increased membrane permeability in preterms, reduced albumin so more free drug, greater water content

351
Q

factors affecting metabolism in children

A

different metabolites, enzyme systems still developing up to 10 years, excess bilirubin competes

352
Q

factors affecting excretion in children

A

reduced GFR, reduced tubular secretion

353
Q

behavioural drug-drug interactions

A

alters patients behaviour to modify compliance with another drug

354
Q

pharmaceutic polypharmacy

A

formulation of one drug is altered by another before administration

355
Q

distributive shock

A

anaphylactic
neurogenic
septic

356
Q

pharmacodynamic polypharmacy

A

interacting drugs have either additive or opposite effects

357
Q

pharmacogenomics

A

studies to identify genes involved in determining responsiveness to a given drug and to distinguish who will respond to specific drugs

358
Q

signs of shock

A

increased HR, CRT and RR

decreased BP, spO2, conscious level, urine output and pH level

359
Q

shock definition

A

acute circulatory crisis caused by any reduction in blood flow, marked by tachycardia and hypotension

360
Q

3 stages of shock

A

1) compensatory - arterial pressure and tissue perfusion reduced, compensatory mechanisms activated to maintain perfusion to the heart and brain
2) progressive stage - begins as compensatory mechanisms fail to maintain CO and tissues become hypoxic due to poor perfusion
3) irreversible stage - as shock progresses, permanent organ damage occurs as compensatory mechanisms can no longer maintain CO

361
Q

why is vitamin K given at birth and then at 7 days?

A

to help with blood clotting

362
Q

cardiogenic shock

A

inadequate pump or increased demand on heart

363
Q

distributive shock

A

anaphylactic
neurogenic
septic

364
Q

Embryological development of heart

A

day 20 - endothelial tubes begin to fuse
day 22 - heart starts pumping
day 24 - heart continues to elongate and starts to bend
day 28 - bending continues as ventricle moves caudally and atrium moves cranially
day 35 - bending is complete

365
Q

pathophysiology of heart failure

A

trigger event reduces ability of myocardium to contract –> reduction in cardiac output –> sympathetic nervous system responds or RAA system is activated

366
Q

effect of RAA system being activated in heart failure

A

high levels leads to further myocardial injury

367
Q

how does sympathetic system respond to heart failure?

A

releases noradrenaline to maintain MAP and organ perfusion

368
Q

effects of underproduction of stress hormones

A

hypoglycaemia, weakness, hypotension, PTSD like effects

369
Q

signs of heart failure in adolescents

A 
fatigue + exercise intolerance
SOB and tachypnoea
low BP
abdo pain
oliguria
pitting oedema
370
Q

staging of heart failure

A

1) aymptomatic
2) mild tachypnoea or diaphoresis with feeding
3) mared tachypnoea or diaphoresis with feeding. prolonged feeding times with growth failure, mearked dyspnoea or exertion in older children.
4) tachypnoea, recession, grunting ot diaphoresis at rest

371
Q

investigations for heart failure

A 
CXR
ECG
echocardiography
cardiac catheterisation
exercise stress test
372
Q

medications used in heart failure

A

ACE inhibitors, B blockers, inotropes, vasodilators, diuretics.

373
Q

Stress response - alarm phase

A

occurs in seconds, lasts minutes
fight or flight response

  • increased O2 and energy availability
  • divert blood to required tissues
  • enhance senses
  • immune changes
  • activate sympathetic nervous system
374
Q

stress response - resistance phase

A

cope with ongoing demands
lasts for hrs/days/yrs

mainly hormonal, maintains body in survival mode

growth hormone - increased lipolysis to free fatty acid as energy source, increased glucose availability
thyroid hormone - increased glucose breakdown to produce ATP
cortisol - increased glucose availability, maintain vascular and renal functions, suppresses immune system, feedsback to CNS

375
Q

effects of overproduction of stress hormones

A

hyperglycaemia, tissue wastage, insulin resistance, cardiovascular changes, anxiety, psychosis, immunosuppression

376
Q

effects of underproduction of stress hormones

A

hypoglycaemia, weakness, hypotension, PTSD like effects

377
Q

medication for type 2 diabetes

A

sulfonylureas which stimulate beta cells to produce more insulin

378
Q

alpha islets of langerhans

A

secrete glucagon

379
Q

descending pain pathway

A

signal from periaqueductal grey matter travels to nucleus raphe magnus and synapses with 2nd neuron. Travels to dorsal horn of spinal cord. This neuron should control communication between 1st and 2nd order neuron to help control pain signals.

380
Q

delta islets of langerhans

A

secrete somatostatin produced by other endocrine cells

381
Q

normoglycaemia cycle

A

increased blood glucose –> pancreas releases insulin which stimulates glycogen formation in liver and stimulates glucose uptakes by cells –> blood glucose falls to normal range

382
Q

symptoms of diabetes

A

hyperglycaemia, hypoglycaemia, polyuria, polydispia, glycosuria, pruritis

383
Q

type 1 diabetes

A

irreversible autoimmune destruction of the islets of langerhans - body cannot produce insulin

384
Q

type 2 diabetes

A

secondary decline in insulin secretions by islets of langerhans
can produce insulin but no enough or it doesn’t work properly due to a resistance to glucose

385
Q

medication for type 2 diabetes

A

sulfonylureas which stimulate beta cells to produce more insulin

386
Q

ascending pain pathway

A

Cell damage leads to prostaglandin release. Sensory nerve fibres carry this signal to the dorsal horn of the spinal cord (1st order neuron). Relayed to 2nd order neuron which carries the signal to the spinothalamic tract and ascends through the spinal cord, brain stem and terminates in the thalamus (relay station). 2nd order synapses with 3rd order which relays to cortex that receives pain.

387
Q

descending pain pathway

A

signal from periaqueductal grey matter travels to nucleus raphe magnus and synapses with 2nd neuron. Travels to dorsal horn of spinal cord. This neuron should control communication between 1st and 2nd order neuron to help control pain signals.

388
Q

Af fibers pain

A

fast, localised sharp pain

389
Q

C fibers pain

A

slow, poorly located pain

390
Q

minimum length of chronic pain

A

3 months

391
Q

glial cells

A

non neuron cells which protect neurons

392
Q

role of glial cells in pain

A

when exposed to neurotransmitters, glial cells are activated and produce chemicals which communicate with afferent pain pathway - stimulates more neurotransmitters which causes more pain (positive feedback cycle)

393
Q

embryology of brain

A

17 days - flat 3 layered embryo
20 days - neural folds to form neural plate
22 days - neural folds close to form neural tube
Week 4 - primary vesicles develop into fore, mid and hind brain
Weeks 5-11 - secondary vesicles develop into diff parts of brain. (week 5) - 2 major flexuses form, causing telencephalon and diencephalon to angle towards brain stem
Week 13 - cerebral hemispheres develop and grow to enclose diencephalon and rostral brain stem

394
Q

role of cerebrum

A

speech, thoughts, emotion, muscle function

395
Q

role of thalamus

A

sensory relay station

396
Q

role of epithalamus

A

endocrine processes

397
Q

role of hypothalamus

A

controls hormone release

398
Q

role of cerebellum

A

physical movement

399
Q

role of hippocampus

A

consolidates short term memory

400
Q

role of amygdala

A

emotions

401
Q

embryology of brain

A

17 days - flat 3 layered embryo
20 days - neural folds to form neural plate
22 days - neural folds close to form neural tube
Week 4 - primary vesicles develop into fore, mid and hind brain
Weeks 5-11 - secondary vesicles develop into diff parts of brain. (week 5) - 2 major flexuses form, causing telencephalon and diencephalon to angle towards brain stem
Week 13 - cerebral hemispheres develop and grow to enclose diencephalon and rostral brain stem

402
Q

neurocranium

A

protective case of skull

403
Q

viscerocranium

A

facial skeleton

404
Q

hepatic encephalopathy

A

loss of brain function as result of failure in the removal of toxins from blood due to liver damage

405
Q

when does posterior fontanelle close?

A

4-6 weeks old

406
Q

growth of brain up to 10 years old

A

doubles by 1 year
75% by 2
90% by 6
100% by 10

407
Q

ionotropic

A

neurotransmitter made of proteins

408
Q

role of occipital lobe

A

vision

409
Q

combination of neurotransmitters with receptors (dopamine, adrenaline, histamine and opioid)

A

dopamine - at least 5 different receptors
adrenaline - alpha and beta receptors
histamine - H1, H2 or H3
opioid - Mu, delta, kappa and ORL1 receptors, involved with pain due to tissue damage

410
Q

hypoxic-ischaemic injury

A

occurs during prenatal, intrapartum or postpartum period where adequate cerebral blood flow is prevented from providing oxygen to the brain.
moderate decrease in cerebral perfusion triggers cerebral arteries to redistribute blood to posterior circulation to maintain adequate perfusion to brain stem, basal ganglia and cerebellum. damage occurs in cerebral cortex and hemispheres.

411
Q

effect of angiotensin converting enzyme inhibitor

A

blood pressure will fall due to vasodilation

412
Q

What term indicates the disability caused by a fracture occurring at L2?

A

paraplegia

413
Q

Where are the stem cells that can become all types of leukaemia produced?

A

red bone marrow

414
Q

role of parietal lobe

A

sensory perception and integration

415
Q

role of temporal lobe

A

cognitive functions and control of voluntary movement or activity

416
Q

role of occipital lobe

A

vision

417
Q

where does the coronary vein drain into?

A

into the great cardiac vein and through the coronary sinus into the right atrium.

418
Q

why can insulin not be given orally?

A

it is a protein so broken down by digestive enzymes (protease)

419
Q

effect of angiotensin converting enzyme inhibitor

A

blood pressure will fall due to vasodilation

420
Q

what are statins used for?

A

to reduce cholesterol levels

421
Q

Where are the stem cells that can become all types of leukaemia produced?

A

red bone marrow

422
Q

What kind of polysaccharide is the main food source of energy for humans?

A

starch

423
Q

ACE inhibitors such as captopril can accidently bind to and block kininase enzymes in the bronchioles – how might this cause the side-effect of a dry cough?

A

levels of bradykinin can build up and irritate the lining of the lungs

424
Q

How may calcium channel blockers such as verapamil cause constipation?

A

inhibit contraction of smooth muscle - reduce peristalsis

425
Q

how does drug get from digestive system to circulation?

A

gut –> hepatic portal vein –> liver –> hepatic vein into circulatory system

426
Q

why can insulin not be given orally?

A

broken down by digestive enzymes

427
Q

transposition of the great arteries

A

where two major vessels leaving the heart do so from the wrong ventricles

428
Q

what are statins used for?

A

to reduce cholesterol levels

429
Q

What lipid is the raw material for steroid hormones?

A

cholesterol

430
Q

What kind of polysaccharide is the main food source of energy for humans?

A

starch

431
Q

Explain the term sympathomimetic.

A

has an adrenergic effect

432
Q

What type of natural chemical messenger would bind to nicotinic and muscarinic receptors?

A

acetylcholine

Year 2 Biopharmacy (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions