201 HI - Disease & Pharmacology Flashcards

1
Q

Immuno- suppressors, immuno-modulators and antibody treatments

A

Induction therapy for transplantation

  • Lymphocyte-depleting agents - Antithymocyte globulin
  • Interleukin 2 receptor antagonists - Basiliximab

Glucocorticoids (corticosteroids)

Antiproliferative immunosuppressants - Azathioprine

Calcineurin inhibitors - Ciclosporin

mTOR inhibitors - Sirolimus

TNF-α inhibitors - Infliximab

Antibodies against CD20 - Rituximab

Interleukin inhibitors - Tocilizumab

Janus kinase (JAK) Inhibitors - Tofacitinib
Immunomodulation therapy	- Interferons, interleukins, IVIG
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2
Q

AE of Glucocorticoids (corticosteroids)

Immuno- suppressors, immuno-modulators and antibody treatments

A

Iatrogenic Cushing syndrome

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3
Q

Antiproliferative immunosuppressants

Immuno- suppressors, immuno-modulators and antibody treatments

A

Azathioprine

  • Activated to 6-mercaptopurine (6-MP)

AE: Bone marrow suppression

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4
Q

Calcineurin inhibitors

Immuno- suppressors, immuno-modulators and antibody treatments

A

Ciclosporin

  • Inhibit calcineurin, which normally activates the transcription of interleukin-2

AE: Hyperlipidaemia, hypertension, gingival hyperplasia, renal dysfunction

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5
Q

mTOR inhibitors

Immuno- suppressors, immuno-modulators and antibody treatments

A

Sirolimus

AE: Myelosuppression

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6
Q

TNF-α inhibitors

Immuno- suppressors, immuno-modulators and antibody treatments

A

Infliximab

AE: Latent TB and other serious infections may recur

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7
Q

Antithrombotic drugs

A

Thrombolytics/fibrinolytics - Alteplase

Heparin - Enoxaparin

Low-molecular-weight heparin - Fondaparinux

Direct thrombin inhibitor - Bivalirudin

Vitamin K antagonist - Warfarin

Direct Oral Anticoagulants (DOACs) - Dabigatran

Antiplatelet drugs:

  • Aspirin
  • P2Y12 antagonists - Clopidogrel (CYP2C19)
  • GPIIb/IIIa Receptor Antagonists - Abciximab
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8
Q

Thrombolytics/fibrinolytics

Antithrombotic drugs

A

Alteplase

  • Enzymically activate plasminogen to give plasmin which digests fibrin and fibrinogen, lysing the clot.

AE: Bleeding

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9
Q

Heparin, low-molecular-weight heparin

Antithrombotic drugs

A

Enoxaparin

  • Binds to AT III → inhibits factor Xa
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10
Q

Vitamin K antagonist

Antithrombotic drugs

A

Warfarin

  • Inhibits the reduction of vitamin K and thus prevents the γ-carboxylation of the glutamate residues in factors II, VII, IX, and X
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11
Q

AE of Direct Oral Anticoagulants (DOACs)

Antithrombotic drugs

A

Bleeding

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12
Q

Haem iron vs non-haem iron

A

Haem:

  • binds to haemoglobin & myoglobin
  • can be found in animal products
  • in ferrous state (Fe2+)

Non-Haem:

  • free iron molecules
  • can be found in plant-based foods
  • in ferric state (Fe3+)
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13
Q

Mechanisms of iron absorption

A
  1. Duodenal cytochrome B reduces Fe3+ → Fe2+ (meat product not needed to be converted)
  2. DMT1 transport Fe2+ into duodenal enterocyte
  3. Ferroportin export iron from enterocyte when needed - Fe2+ released from ferritin stores into blood
  4. Hephaestin converts Fe2+ → Fe3+ - binds to transferrin and transported to target tissues
  5. Fe3+ stored in ferritin
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14
Q

Where does iron absorption mainly occur?

A

Duodenum

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15
Q

How is iron absorption regulated?

A

Hepcidin

  • produced in the liver in response to increased iron load & inflammation
  • binds to ferroportin and causes degradation

High hepcidin levels block intestinal iron absorption

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16
Q

4 main causes of iron deficiency anemia

A

↓ iron intake
↓ iron absorption
↑ demand
↑ loss

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17
Q

Hepcidin levels ______ in iron deficiency

A

decrease

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18
Q

Primary & secondary causes of iron overload

A

Primary:

  • hereditary hemochromatosis
  • iron poisoning

Secondary:

  • blood transfusions
  • iron loading anemias
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19
Q

What causes megaloblastic macrocytic anaemia?

A

Vitamin B12 & B9 (folate) deficiency

20
Q

What is the most common type of anemia?

A

Iron deficiency

21
Q

Iron deficiency can cause _____ anemia

A

hypochromic microcytic

22
Q

How can iron status be assessed?

A

Functional iron
Transported iron
Serum iron

23
Q

Treatment of iron overload

A

Iron chelation

24
Q

Cytotoxic drugs target mechanisms by which?

A

Cells divide & grow and prevents cell from dividing

25
3 main approaches to delivering dose-intense chemotherapy
Dose escalation: increasing dosage Reduction of interval: reduce the time between cycles Sequential dosing: single or combination drugs given sequentially
26
What are the 3 phases of chemotherapy?
Induction Consolidation Maintenance
27
Hematological malignancies (3)
Leukaemia - cancer which starts usually in bone marrow 白血病 Lymphoma - cancer that begins in lymphocytes 淋巴瘤 Myeloma - cancer that forms in plasma cells 骨髓瘤
28
MOA of Vincristine (for Acute Lymphoblastic Leukemia)
Inhibits microtubule assembly - disrupts M-phase
29
Chronic leukaemia
Lots of partially developed WBC over a long period of time
30
Chronic Myeloid Leukaemia (CML) vs Chronic Lymphoblastic Leukaemia (CLL)
CML affects granulocytes - neutrophil, basophil, eosinophil - cells divide too quickly CLL affects lymphocytes - cells don't die as they should
31
Why are chemotherapy drugs often used in combination?
To provide maximum cell kill within the range of toxicity To broaden the range of interaction between drugs & tumor cells To prevent or slow the development of cellular drug resistance
32
Sepsis
A life-threatening condition that arises when the body's response to an infection injures its own tissues & organs
33
Septicaemia
Septicaemia is when bacteria enter the bloodstream, and cause blood poisoning which triggers sepsis
34
What is SIRS (Systemic inflammatory response syndrome)?
A non-specific clinical response with 2 or more objective signs of systemic inflammation 全身炎症反應綜合症
35
What is sepsis in the setting of SIRS?
SIRS w a presumed or confirmed infectious process Infection associated w organ injury distant from the site of infection
36
Is it required to have a confirmed infection to confirm sepsis?
No | - only ~60% of confirmed cases are w confirmed infections
37
Role of endothelium
Maintains homeostasis between coagulation & fibrinolysis
38
How does septic shock occur?
Sepsis increases nitric oxide levels | → leading to excessive vasodilation & refractory hypotension
39
When to prescribe antibiotic for sepsis pt?
ASAP - don't wait for culture, use broad spectrum antibiotic - re-evaluate choice of antibiotics after culture data available
40
The "sepsis six" bundle
1. Give high flow oxygen 2. Start intravenous fluid resuscitation 3. Take blood cultures 4. Give intravenous antibiotics 5. Measure lactate and FBC 6. Monitor accurate hourly urine output
41
What is the target of HIV?
CD4+ lymphocytes | - cluster of differentiation protein 4
42
How many copies of RNA does each HIV virion contain?
2
43
Opportunistic infections
An infection caused by a pathogen that does not normally produce disease in a healthy individual
44
Threshold of CD4+ to worry about opportunistic infections
<200 cells/mm3
45
Causative agent of Kaposi's sarcoma
Human herpes virus 8
46
Causative agent of non-Hodgkin's lymphoma
Epstein-Barr virus