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ICS Overview Flashcards

1
Q

Tumour grading, what do stages 1, 2 and 3 mean?

A

1- Well differentiated
2- Moderately differentiated
3- Poorly differentiated
(how well it resembles original histology)

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2
Q

Name 5 causes of acute inflammation

A

Microbial infection
Hypersensitivity
Trauma/ Heat/ Cold
Chemical irritants
Bacterial toxins
Ischaemic necrosis

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3
Q

How does acute inflammation present? [5]

A

Rubor-redness
Calor-heat
Tumour-swelling
Dolor-pain
Loss of function

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4
Q

Carcinogens:
Asbestos causes …….
HPV causes……
UV causes …..
EBV causes …..
Rubber causes ……
Soot causes ……

A

Asbestos causes mesothelioma
HPV causes cervical cancer
UV causes skin cancer
EBV causes Burkitt’s lymphoma
Rubber causes bladder cancer
Soot causes scrotal cancer

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5
Q

Define apoptosis

A

Non-inflammatory, programmed and defined sequence of intracellular events leading to remove of a cell without release of harmful products

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6
Q

What are the 4 possible outcomes of acute inflammation?

A

Resolution
Supparation
Organisation
Progression

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7
Q

Intrinsic pathway of apoptosis:
BAX acts on […] to promote […] release. This activates […] which results in apoptosis.

A

BAX acts on mitochondrial membrane to promote cytochrome c release. This activates CASPASES which results in apoptosis.

Bax and Bak are members of the Bcl-2 family and core regulators of the intrinsic pathway of apoptosis. Upon apoptotic stimuli, they are activated and oligomerize at the mitochondrial outer membrane (MOM) to mediate its permeabilization, which is considered a key step in apoptosis. Cytochrome c is one of the mitochondrial proteins that is released into the cytosol when the cell is activated by an apoptotic stimulus.
Caspases are a family of endoproteases that provide critical links in cell regulatory networks controlling inflammation and cell death.

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8
Q

Arterial thrombosis:
It begins with an […] that may have a fatty streak. It grows and […]. This causes […] in the intima. This causes […] and […]. RBCs get trapped in fibrin mesh. More protrusion, more disruption, more platelets, positive feedback.

A

Arterial thrombosis:
It begins with an atheromatous plaque that may have a fatty streak. It grows and disrupts flow. This causes cell death in the intima. This causes fibrin deposition and platelet clumping. RBCs get trapped in fibrin mesh. More protrusion, more disruption, more platelets, positive feedback.

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9
Q

Name 2 inducers of apoptosis

A

Glucocorticoids
Free radicals
Ionising radiation
DNA damage

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10
Q

What is the goal of Ca channel blockers and how is it achieved?
Give an example of one!

A

Anti-hypertensive by decreasing Ca available to heart muscles, therefore decreases ionotropy
Amlodipine, Verapamil

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11
Q

DOACs, what does it stand for?
Give an example of one!
How do they work?

A

Direct oral anti-coagulants
apiXaban, rivaroXaban
They act on active clotting factor X (10)

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12
Q

Very briefly, what do ACE inhibitors aim to do and how do they achieve it?
Give an example of one!

A

Anti-hypertensive via inhibiting ACE and therefore RAAS system which aims to retain water
Ramipril

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13
Q

What do B2 agonists do?
Give an example and what it treats!

A

Bronchodilation
SABAs (salbutamol) for COPD

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14
Q

What immune cells are involved in acute inflammation?

A

neutrophils and monocytes

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15
Q

What’re the 2 main routes of drug administration?

A

Systemic and Local

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16
Q

What is alteplase used to treat?

A

Ischaemic strokes

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17
Q

What do B1 agonists do?
Give an example of one and what it treats!

A

Increase ionotropy and chronotropy of the heart (force and HR)
Dobutamine?
Treats cardiogenic shock

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18
Q

Outcomes of Acute Inflammation, Organisation:
This is when the site is replaced by […] tissue. New […] grow in the exudate, […] migrate and […] occurs.

A

Outcomes of Acute Inflammation, Organisation:
This is when the site is replaced by granulation tissue. New capillaries grow in the exudate, macrophages migrate and fibrosis occurs.

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19
Q

Connective tissue tumours: What tissue do these involve?
Lipoma
Rhabdomyoma
Leiomyoma
Chrondroma
Osteoma
Angioma
Neuroma

A

Adipocytes
Striated muscle
Smooth muscle
Cartilage
Bone
Vascular
Nerves

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20
Q

What is the main symptom of opioid overdose?
How is opioid overdose treated?
What is the route of administration?

A

Respiratory depression
Treated with naloxone intravenously

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21
Q

Name 3 complications of athersclerosis!

A

Cerebral infarct
MI
Peripheral Vascular Disease
Carotid atheroma-> TIAs
Aortic aneurysm
Gangrene

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22
Q

What’re the 3 parts of Virchow’s Triad? Name 3 examples for each!

A

Reduction in blood flow- Atrial Fib, Varicose, Immobility, Ventric/venous insuff., Venous obstruction i.e pregnant
Blood vessel injury- Trauma, Surgery, Hypertension, Invasive procedures, Nicotine
Increased coaguability- Sepsis, Smoking, Malignancy, Coagulation disorders, Liver damage

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23
Q

Extrinsic pathway of apoptosis:
[…] or […] binds to CSM receptors. This results in […] activation and therefore apoptosis.

A

Extrinsic pathway of apoptosis:
FASL or TNF-L binds to CSM receptors. This results in caspase activation and therefore apoptosis.

Fas and FasL are both members of the tumour necrosis factor (TNF) family; Fas is part of the transmembrane receptor family and FasL is part of the membrane-associated cytokine family. When the homotrimer of FasL binds to Fas, it causes Fas to trimerize and brings together the death domains (DD) on the cytoplasmic tails of the protein.

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24
Q

In non-competitive inhibition, the curve shifts […]. The drug has […] affinity, […] efficacy, its […] potent, and the EC50 is […].
Can a maximal response be achieved with a high enough drug dose? […]

A

In non-competitive inhibition, the curve shifts down and right. The drug has less affinity, less efficacy, its less potent, and the EC50 is decreased.
Can a maximal response be achieved with a high enough drug dose? NO
NO because some receptors are MIA and can’t be used to achieve max response

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25
Q

Carcinomas tend to metastasise via […]
Sarcomas tend to metastasise via […]

A

Carcinomas tend to metastasise via lymphatics
Sarcomas tend to metastasise via haematogenous spread
Carcinoma~ skin/ cells lining internal organs (epithelial)
Sarcoma~ connective tissue (fat/ blood vessles/ nerves/ bones/ muscles)

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26
Q

What cancer never metastasises?

A

Basal cell carcinoma

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27
Q

Why doesn’t atheroma occur in veins?

A

lower blood pressure

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28
Q

Name 5 causes of chronic inflammation and an example for each!

A

Resisting infecting agent- TB
Endogenous material- Necrosis tissue
Exogenous material- Asbestos
Autoimmune disease- Rheumatoid
Prim. granulomatous disease- Crohn’s
Transplant rejection

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29
Q

Metastasis:
It begins with […] from primary tumour. Then […] into vessel lumens. Whilst in the blood it evades […]. It then […] at a remote location. From here […] occurs, allowing it to exit the vessel into new tissue. The tumour then proliferates.

A

It begins with detachment from primary tumour. Then intravasation into vessel lumens. Whilst in the blood it evades the host’s defence. It then adheres to endothelium at a remote location. From here extravasation occurs, allowing it to exit the vessel into new tissue. The tumour then proliferates.

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30
Q

Define atrophy and give an example of it!

A

No. or size of cells decreases
In diseases like ALS

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31
Q

Define hyperplasia and give an example of it!

A

Increased no. of cells (via mitosis)
Bone marrow hyperplasia in those living at high altitude

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32
Q

In competitive inhibition, the drug has […] afffinity, […] efficacy, […] EC50 and the drug is […] potent.
Will the response eventually be maximal if the drug dose is increased enough? […]

A

In competitive inhibition, the drug has less afffinity, the same efficacy, the same EC50 and the drug is less potent.
Will the response eventually be maximal if the drug dose is increased enough? YES

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33
Q

Define metaplasia and give an example of it!

A

Change from one cell type to another
Barret’s Eosophagus
(squamous epi. to columnar epi.)

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34
Q

Define thrombosis

A

Solidification of blood contents in vascular system throughout life

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35
Q

Small emboli may cause […].
Large emboli can cause acute […] [2] problems which present as […] [2].
Massive emboli are often caused by […]

A

Small emboli may cause idiopathic pulmonary hypertension.
Large emboli can cause acute resp/cardio [2] problems which present as chest pain and shortness of breath [2].
Massive emboli are often caused by long thrombi in leg veins.

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36
Q

If a tumour is malignant, what prefix/ suffix is it given?

A

Sarcoma

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37
Q

What is a carcinoma?
Malignant or benign?

A

Tumour of epithelial cells
Malignant

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38
Q

Arterial vs Venous Thrombosis:
Cause?
BP?
Main Constituent?
Complications [2]?
Treatments+i.e?

A

Atheroma vs Stasis
High vs Low
Platelets vs RBCs
MI/Stroke vs DVT/PE
Anti-platelets (aspirin) vs anti-coagulants (warfarin)

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39
Q

What are the 5 type of blood thinners

A

DOACs (direct oral anticoag)
Warfarin
LMWH
Alteplase
Antiplatelets

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40
Q

LMWH (blood thinners), what does it stand for?
How do they work?

A

Low molecular weight heparin
Inhibits clotting factors 3 and 10

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41
Q

When are beta blockers contraindicated?

A

Absolute asthma in patient

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42
Q

What are the treatments for paracetamol overdose? How does this combination work?

A

Activated charcoal then acetylcystine
Activated charcoal lines the stomach to protect it, then acetylcystine mops up the paracetamol/toxic products

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43
Q

Benign vs Malignant tumours:
Invade BM?
Exo/Endophytic?
Mitotic activity?
Circumscribed?
Necrosis & Ulceration?
Resemblance to norm tissue?

A

No vs Yes
Exo vs Endo
Low vs High
Well vs Poorly
Rare vs Common
High vs Low

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44
Q

Outcomes of Acute Inflammation, Supparation:
This is when […] forms and is enveloped by a […] membrane. There may also be scarring.

A

Outcomes of Acute Inflammation, Supparation:
This is when pus forms and is enveloped by a pyogenic membrane. There may also be scarring.

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45
Q

What is a granuloma?
3 diseases that cause them?

A

An aggregrate of epithelioid histocytes (Macrophages that mimic epithelial cells and form tight cell junctions)
TB, Leprosy, Crohn’s & Sarcoidosis

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46
Q

What is a mural thrombus?

A

One that attaches to vessel wall (large like aorta) or cardiac chambers

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47
Q

Define infarction

A

Cell death caused by ischaemia

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48
Q

Apoptosis vs Necrosis
Inflammatory?
Organelles go where?
CSM status?
Chromatin status?

A

No vs Yes
Stay in cell vs Splurge out
Intact vs Damaged
Unaltered vs Altered

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49
Q

What is a carcinogen

A

An environmental agent participating in the cause of tumours

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50
Q

Acute inflammation:
Vasodilation results in increased blood volume and vascular […]. This results in the formation of a cellular exudate which leads to emigration of […]. Initially, they arrive at the site due to […] plasma viscosity and […] blood flow. Then they […] in […], this is called pavementing. From here they exit the vessel and enter surrounding tissue. Diapedesis may occur, this is a […] process indicative of […].

A

Vasodilation results in increased blood volume and vascular permeability. This results in the formation of a cellular exudate which leads to emigration of neutrophil polymorphs. Initially, they arrive at the site due to increased plasma viscosity and slower blood flow. Then they adhere to endothelium in venules, this is called pavementing. From here they exit the vessel and enter surrounding tissue. Diapedesis may occur, this is a passive process indicative of severe vascular injury.

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51
Q

Outcomes of Acute Inflammation, Resolution:
Restoration of tissues?
Cell death?
Fate of causative agent?

A

Complete restoration
Minimal cell death
Rapid destruction of causative agent

52
Q

Which gene arrests the cell cycle and initiates DNA repair?

A

p53

53
Q

What is an embolism?

A

A mass of material in vascular system, able to lodge in vessles and block system

54
Q

Arterial embolism:
Where can they travel to?
Which ones can travel anywhere?

A

Anywhere downstream of entry point
Mural thrombi in LV

55
Q

What stain is TB identified with?

A

Ziehl-Neelsen Stain

56
Q

Venous thrombosis:
Thrombi begin at […]. They produce turbulence and are damaged. When […] falls, […] also slows and thrombi can form. This would present with […] [3]

A

Venous thrombosis:
Thrombi begin at valves. They produce turbulence and are damaged. When BP falls, BF also slows and thrombi can form. This would present with tenderness, redness and swelling. [3]

57
Q

Name 3 preventions for atherosclerosis!

A

Stop smoking
Weight loss
Low dose aspirin
Statins

58
Q

NSAID mechanism:
They work by inhibiting the […] pathway which involves […]. [2]

A

They work by inhibiting the arachidonic pathway which involves COX-1 and COX-2. [2]

59
Q

Define necrosis

A

Inflammatory, traumatic cell death

60
Q

Which pathway of apoptosis is used by the immune system and what is it used to do?

A

Extrinsic, to eliminate lymphocytes

61
Q

Gangrene:
This is when you have necrosis + […]. It appears […] due to deposition of […] from […].

A

This is when you have necrosis + rotting tissue. It appears black due to deposition of iron sulphate from Hb degradation.

62
Q

What cytokines are produced by macrophages in chronic inflammation?

A

Interferon alpha and beta
Interleukins 1, 6 & 8
TNF-alpha

63
Q

What’re the 4 outcomes of a thrombus forming? Explain them too!

A

Resolved- Thrombi cleared
Organised- Becomes scar and narrows lumen
Recanalisation- Intimal cells proliferate, capillaries grow into thrombus and fuse to form bigger vessels
Embolus- Fragment of thrombus breaks off into circulation

64
Q

Define hypertrophy and give an example of it!

A

Increased cell size (w/o increase in no.)
Uterine hypertrophy in pregnancy

65
Q

Arterial thrombosis:
It begins with an atheromatous plaque that may have a […]. It grows and disrupts flow. This causes cell death in the […]. This causes fibrin deposition and platelet clumping. RBCs get trapped in fibrin mesh. More protrusion, more disruption, more platelets, positive feedback.

A

Arterial thrombosis:
It begins with an atheromatous plaque that may have a fatty streak. It grows and disrupts flow. This causes cell death in the intima. This causes fibrin deposition and platelet clumping. RBCs get trapped in fibrin mesh. More protrusion, more disruption, more platelets, positive feedback.

66
Q

Define dysplasia and give an example!

A

Abnormal change in cell type
Progression to becoming cancer

67
Q

Name 5 athersclerosis risk factors!

A

Hypercholesterolaemia!
Smoking
Hypertension
Diabetes
Male
Increasing age

68
Q

What is a papilloma?
What is an adenoma?
Are they beningn or malignant?

A

Papilloma= Non-glandular tissue
Adenoma= Secretory tissue
Both are benign

69
Q

What are the 4 types of necrosis?

A

Coagulative
Liquefactive
Caseous
Gangrene

70
Q

Atherosclerosis:
Endothelial cell damage/dysfunction intitiates this process. This causes […] to accumulate in arterial wall. […] head to the site and take up […] to form […] cells. At this point the […] forms. Activated macrophages release […] and […]. […] proliferates around lipid core and a […] cap forms. This then […] and the process repeats elsewhere.

A

Atherosclerosis:
Endothelial cell damage/dysfunction intitiates this process. This causes LDLs to accumulate in arterial wall. Macrophages head to the site and take up lipids to form foam cells. At this point the fatty streak forms. Activated macrophages release cytokines and growth factors. Smooth muscle proliferates around lipid core and a fibrous collagen cap forms. This then ruptures and the process repeats elsewhere.

71
Q

Acute inflammation:
Vasodilation results in increased blood volume and vascular permeability. This results in the formation of a cellular exudate which leads to emigration of neutrophil polymorphs. Initially, they arrive at the site due to increased plasma viscosity and slower blood flow. Then they adhere to endothelium in venules, this is called […]. From here they exit the vessel and enter surrounding tissue. […] may occur, this is a passive process indicative of severe vascular injury.

A

Vasodilation results in increased blood volume and vascular permeability. This results in the formation of a cellular exudate which leads to emigration of neutrophil polymorphs. Initially, they arrive at the site due to increased plasma viscosity and slower blood flow. Then they adhere to endothelium in venules, this is called pavementing. From here they exit the vessel and enter surrounding tissue. Diapedesis may occur, this is a passive process indicative of severe vascular injury.

72
Q

Define carcinogenesis

A

Transformation of normal cells to neoplastic cells via permanent mutation/genetic alteration

73
Q

What does each immune cell do in chronic inflammation?

A

B lymphocytes- Become plasma cells and make antibodies
T lymphocytes- Cell mediated immunity
Macrophages- Respond to chemotactic stimuli and produce cytokines

74
Q

What does it mean if you have a granuloma with eosinophils present?

A

Presence of a parasite

75
Q

Define neoplasm

A

Autonomous, abnormal, persistent new growth
(CANCER)

76
Q

Name 4 signs of chronic inflammation!

A

Fibrosis
Necrosis
Signs of continued destruction
Granulomatous inflammation
Chronic ulcer
Chronic abcess cavity (pus)
RARELY exudation

77
Q

Coagulative necrosis:
This is the […] common type. It occurs in […] organs. It is caused by […].

A

Coagulative necrosis:
This is the most common type. It occurs in most organs. It is caused by ischaemia.

78
Q

What is an adenocarcinoma?

A

Tumour made up of epithelial (carcinoma) secretory tissue (adenoma)

79
Q

Liquefactive necrosis:
It occurs in […]. It is caused by […].

A

Liquefactive necrosis:
It occurs in the brain. It is caused by a lack of substantial supporting stroma.

80
Q

What is progression in outcomes of acute inflammation?

A

This is when the causative agent is not removed therefore causing chronic inflammation.

81
Q

Caseous necrosis:
This necrosis is identified by […]. A disease that causes this is […].

A

Caseous necrosis:
This necrosis is identified by the cheese pattern. A disease that causes this is TB.

82
Q

How does arterial thrombosis present?

A

Loss of pulse distal to thrombus
Cold, pale, painful area
Gangrene

83
Q

What do the letters stand for in TNM staging?
What are the numbers/letters for each one?

A

T- Size (0,1,2,3,4,X)
N- Lymph node status (0,1,2,X) <– none, some, all, unmeasurable
M- Metastasis (0,1,X)

84
Q

Name 2 inhibitors of apoptosis

A

Growth factors
Extracellular cell matrix
Sex steroids

85
Q

What immune cells are involved in chronic inflammation?

A

lymphocytes
macrophages
plasma cells

86
Q

What do carcinogenic and oncogenic mean?

A

Cancer causing
Tumour causing

87
Q

What is the main side effect of opioids?

A

constipation

88
Q

What are the 3 types of diuretics (based on mode of action)?
Give an example of each!

A

Loop diuretic - Furosemide
Thiazide diuretic - Bendroflumethiazide
Aldosterone antagonist - Spironolactone

89
Q

Adverse drug reactions, ABCDEF. What does each letter stand for and give an example?

A

Augmented (common) i.e dry cough from ACE inhib
Bizarre (unexpected) i.e face itch steroids
Chronic (time related) i.e osteoporosis on steroids
Delayed (dose related) i.e symptom that arises after long term use, thalidomide
End of use (withdrawals)
Failure, reactions due to drug interactions

90
Q

Give an example of a PPI!

A

lanzoprazole, omeprazole
proton pump inhibitor?

91
Q

Define affinity, efficacy and potency

A

-How well a ligand binds to receptor
-How well a ligand ACTIVATES a receptor
-Relative strength of the drug

(potency is solely comparative, i.e drug A vs B. Efficacy, is what % of bound drugs activate the receptor)

92
Q

Parasympathetic NS:
Presynaptic uses?
Postnaptic uses?

A

ACh for both

93
Q

What type of liver failure does paracetamol cause?

A

Acute forminant liver failure

94
Q

In dose/response curves, a shift right indicates […] affinity. Does it indicate an effect on the efficacy? […]

A

In dose/response curves, a shift right indicates lower affinity. Does it indicate an effect on the efficacy? NO

95
Q

Cholinergic pharmacology:
The 2 main receptors are […]. […] are usually presynaptic and […] are usually postsynaptic.

A

Cholinergic pharmacology:
The 2 main receptors are nicotinic and muscarinic. Nicotinic are usually presynaptic and muscarinic are usually postsynaptic.

96
Q

Sympathetic NS:
Presynaptic uses?
Postsynaptic uses?

A

ACh
NAd

97
Q

Name an example of an anti-platelet!

A

Clopidogrel
Ticagrelor
Aspirin

98
Q

Where are Alpha1&2 receptors found?
Give an example of an Alpha blocker and what does it treat?

A

In vessels and sphincters (generally in distal circulation/regions)
i.e bladder neck
tamsulosin for benign prostatic hyperplasia, lets urine flow

99
Q

When seeing adverse drug reactions, how do you respond!

A

Report to MRHA using the yellow card scheme!

100
Q

What is the 1st line treatment for anaphylaxis?
(drug, dose and route)

A

Adrenaline
500micrograms
IM

101
Q

Define bioavailability
Which route of drug administration has 100% BA?

A

The amount of a drug taken up systemically for effect.
IV as the drug doesn’t face any metabolism, goes straight through bloodstream.

102
Q

What does pharmacodynamics refer to?
What does pharmacokinetics refer to?

A

Action of the drug on the body
Action of the body on the drug i.e how its broken down

103
Q

What is the therapeutic range of a drug?

A

The upper and lower bounds of safe doses of drug.
(anything below the threshold is likely to be subtherapeutic and anything above is likely to be toxic)

104
Q

How and where do thiazide diuretics work?

A

They inhibit Na-Cl co-transporter in the DCT

105
Q

Name the 3 main muscarinic receptors and where they’re found!

A

M1- Brain
M2- Heart
M3- Lungs

106
Q

Paracetamol overdose:
This is caused by the liver being forced to used more phase […] metabolism as the phase […] pathway is fully saturated. This means that a lot of […] is produced, which is toxic to the liver.

A

This is caused by the liver being forced to used more phase 1 metabolism as the phase 2 pathway is fully saturated. This means that a lot of NAPQI is produced, which is toxic to the liver.

107
Q

Name 5 conditions that blood thinners are used for!

A

DVT
PE
Atrial Fib
Prosthetic valves
Bleeding disorders
Ischemic stroke
MI

108
Q

When describing pharmacokinetics, ADME is used, what does it stand for?

A

Administration route
Distribution (how well distributed)
Metabolism (i.e IV skips 1st pass metabolism)
Excretion (hepatic or renal)

109
Q

What do B1 antagonists do?
GIve an example and what it treats!

A

Decrease ionotropy and chronotropy of the heart
Propanalol
Hypertension med?

110
Q

How and where do aldosterone antagonists work?

A

They act on the CD (colllecting duct) and inhibit aldosterone. This increases Na+ excretion (but also retains K+)

111
Q

Name 2 examples of NSAIDs

A

Ibuprofen
Naproxen
Celecoxib

112
Q

What is the main effect/goal of a corticosteroid?
Give an example of a corticosteroid!

A

Decrease inflammation
Prednisolone

113
Q

Define agonist and antagonist (in terms of affinity, efficacy and activation of receptor)

A

Agonist: Have full affinity and efficacy, increasing activation of the receptor
Antagonist: Full affinity and ZERO efficacy, thereby decreasing the activation of the receptor

114
Q

What are the 2 systemic routes of drug administration and give an example of each!

A

Enteral (GI Tract) i.e Oral/Rectal
Par-enteral (Not GI) i.e IV/IM

115
Q

How and where do loop diuretics work?

A

They act on the ascending loop of henle and inhibit NKCC2 channels, this stops Na, K and Cl reabsorption.

116
Q

In hepatic drug metabolism, phase 1 and 2 reactions occur.
What types of reactions are they (conjugation or not)?
What is the aim of each phase?
How does it achieve this?

A

Non-conjugation vs conjugation
Slightly vs massively increase hydrophilicity
Using microsomal enzymes like CYP450 vs other process like glucoronidation

117
Q

What is an EC50?

A

The concentration of a drug required to achieve half of the maximum response possible, based on circumstances
i.e non-comp. inhibitors change the maximum response possible

118
Q

What do COX-1 enzymes do?

A

Involved in prostoglandin synthesis which is involved in protecting gastric mucosa. (i.e NSAIDs cause stomach ulcers)

119
Q

In renal drug metabolism, what type of molecules are dealt with and why?

A

Simple molecules as they’re already soluble and can be peed out.

120
Q

Drug metabolism occurs in what 3 systems/places?

A

Kidney
GI tract
Liver

121
Q

At neuromuscular junctions, what NT is used?

A

ACh

122
Q

[…]% of paracetamol undergoes phase 2 metabolism.
[…]% undergoes phase 1.

A

95% of paracetamol undergoes phase 2 metabolism.
5% undergoes phase 1.

123
Q

What do COX-2 enzymes do?
Give an example of a COX-2 selective inhibitor!
Why isn’t it used that much?

A

They are the targeted pathway of NSAIDs.
Activating this pathway causes inflammation (so inhibiting it is anti-inflammatory)
Celecoxib
Not that effective and expensive

124
Q

How does warfarin work as a blood thinner?

A

It inhibits vitamin K production
Therefore no vit K available to make clotting factors 10, 9, 7 and 2

125
Q

Opioids have a […]% bioavailability when taken orally.

A

Opioids have a 50% bioavailability when taken orally.

126
Q
A

Haroon flashcards (10 decks)

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