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MD1 FBS > CSL > Flashcards

CSL Flashcards

1
Q

What is a common marker used to differentiate lymphoblastic leukaemia from myeloblastic leukemia?

A

TdT

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2
Q

What is a common marker used to differentiate myeloid leukemia from lymphoblastic leukemia?

A

Myeloperoxidase and the presence of auer rods

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3
Q

What is a philidephia chromosome and what does it mean for the prognosis of B lymphoblastic leukaemia?

A

translocation between chromosomes 9 & 22, normally occurs in adults and leads to a poor prognosis :(

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4
Q

What is the difference between a lymphoma and a lymphoblastic leukemia?

A

Lymphoma= malignant cells form a mass, mainly in lymph nodes Leukemia- malignant cells in blood

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5
Q

A translocation between chromosomes 15 and 17 is associated with what subtype of leukaemia?

A

acute promyelocytic leukemia

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6
Q

What are the causes of pancytopenia?

A
  1. Autoimmunity against blood cells 2. Drugs (chemotherapy) 3. Inability of cells to be made due to physical limitations e.g. leukaemia –> excess blast formation –> not enough room in marrow for other cells to be made, osteopetrosis (bone hardening)
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7
Q

What are the clinical consequences of failure of blood cell production?

A

Pancytopenia:
Low RBC’s –> anaemia

Low WBC’s –> infection

Low platelets –> inability to clot; easy bruising etc.

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8
Q

Describe the physiology of blood production

A
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9
Q

What is Imatinib?

A

To treat BCR-ABL fusion –> tyrosine kinase inhibitor, used to treat CML and some cases of ALL in cases with a philidephia chromosome mutation t(9;22)

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10
Q

Describe the laboratory diagnosis of leukaemia and the significance of the prognostic markers

A

After taking a bone marrow aspirate, the cells are immunophenotypes (looking for specific cell markers such as CD10, TdT etc) and cytogenetics (chromsome anaylsis). Morphology is also looked at e.g. a blood smear, checking for presence of auer rods to suggest a myeloid blastic lineage.

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11
Q

Who would be a suitable donor for Max? Which represent the genes for the different MHCI and MCHII proteins?

A

Anna and Lachlan

MCHI= HLA-A, B ,C

MCHII- DP DQ DR

  • with aplha and beta chains
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12
Q

Describe what would happen if a patient was given the wrong blood type?

A

Type 3 delayed immune complex hypersensitivity response within 7+ days (adaptive immune response against foreign antigen)

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13
Q

Describe the normal menstrual cycle and ovulation

A
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14
Q

What is the main fx of inhibin in the female reproduction cycle?

A

Inhibition of FSH during the late follicular phae, ovulation and luteal phase to prevent the growth of excess folicle and release of multiple eggs throughout the cycle.

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15
Q

describe normal spermatogenesis

  • include LH and FSH targets and effects
  • pathway from spermatogonium to spermatozoa
A

GnRH –> LH –> leydig cells –> testosterone –> sex characteristics, spermatogenesis

GnRH –> FSH –> sertoli cells –> spermatocyte maturation

Spermatogonium –> primary spermatocyte –> secondary spermatocyte –> spermatid –> spermatozoa

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16
Q

describe normal fertilisation

A
  1. Sperm capacitation occurs in the vagina
  2. Day 1- Fertilisation- Sperm and oocyte meet in fallopian tube –> zygote
  3. Days 2-3- cell division
  4. Days 4-5 Blastocyst reaches uterus
  5. Days 5-9 blastocyst implants
17
Q

Describe normal impantation

Include the formation of the embryo and what cells the baby will grow from.

A

On days 5-9 post fetilisation, the blastocyst adheres to the endometrial lining. Cords of the trophoblastic cells begin to penetrate the endometrium. As these cells divide and conglomerate together, they for synctiotrophoblasts. Unmerged trophoblasts are referred to as cytiotrophoblasts, and act as a barrier between embryo and maternal blood. These cells will go on to become the placenta.
The embryo develops from the inner cell mass of the blastocyst.

18
Q

Describe the normal morphology of sperm in a semen analysis for a fertile male; how many sperm would you expect be be normal % wise?

A

>4% of sperm with normal forms

19
Q

List 2 sexually transmissible infections that can cause infertility

A

Chylmydia

Gonnorhea

20
Q

In which time in pregnancy would teratogenic effects result in major morphological abnormalities?

A

During the embryonic period; weeks 3-8

21
Q

Discuss neonatal/transplacental immunity

A

PASSIVE IMMUNITY

Transplacental- predominately during the third trimester, maternal IgG cross the placenta.

Neonatal- placental IgG stays in the neonate for the first 4-6 months of life. IgA is passed to fetus from breastmilk and protects the immature gut.

22
Q

What are the differences between superficial, partial-thickness (2nd degree) and full-thickness (3rd-degree) burns in terms of:

  • what histological layer of the skin is affected
  • appearance
  • sensation
  • time to heal (scarring?)
  • which types blanch?
A

Blanching: 1st degree, 2nd degree superficial, 2nd degree deep (reduced)

Non-blanching: 3rd degree

23
Q

describe the systemic features of major burns

  • CV
  • Resp
  • Metabolic
  • GI
  • Renal
  • Coagulability
  • Renal
  • Electrolyte imbalance
A
  • CV: dehydration –> hypovolemia –> baroreceptor reflex –>↑ sympathetic activation–> ↑ HR, ↑ vasoconstriction
    • TNF-α release –> ↓ heart contractility –> ↓ CO –> ↓ BP
  • Resp: hypoxia, ↑ sympathetic activation & compensation for metabolic acidosis –> ↑ RR
    • singed nasal hairs –> burned airways –> inflamm mediators –> oedema and bronchoconstrction –> airway obstruction
  • Metabolic: sustained catacholamine release –> catabolic state –> ↑BMR weeks-months following burns
  • GI: vasoconstriction of splanchnic artery –> ischemia of organs
    • curling ulcer –> translocation of microbioto –> TSS
  • Renal ischaemia –> acute tubular necrosis –> ↓ GFR
  • Thermoregulation risk of hypothermia
  • DIC increased coagulability due to hypovolemia –> thick, concentrated blood
  • Electrolytes hyponatremia and hyperkalemia
24
Q

Describe the stem cell niches in the skin

A
  • Basal layer of the epidermis
  • Bulb of the hair follicle
  • In the sebaceous gland
25
Q

Describe how the skin heals after injury

A
26
Q

discuss sources of energy during prolonged strenuous exercise

A

Overtime, increased dependence on aerobic metabolism (1 min sprint= 50% anaerobic, 50% aerobic), with increased utilisation of fats and decreasing glycolysis as CHO stores are depleted overtime.

  • Fastest- ATP stores
  • Faster- Phosphocreatine in muscles
  • Fast- anaerobic glycolysis
  • Slow- Aerobic glycolysis
  • Slowest (sustained efforts)- lipid metabolism; FFA oxidation
27
Q

explain possible underlying mechanisms of fatigue during prolonged, strenuous exercise

A
  • depletion of energy sources, particularly muscle glycogen
  • increased accumulation of fatiging metabolites
    • hydrogen ions, inorganic phosphate, AMP, ADP and IMP.
    • Selective by-products are believed to disturb Na+/K+ balance (hyperkalemia), Ca2+ cycling (↓ Ca2+) and actomyosin interaction, resulting in fatigue
  • reduction in ATP
    • ATP production rates are unable to match ATP utilization rates
  • CNS/neural fatigue
28
Q

Composition of sweat

A

Sweat

  • Hypoosmotic compared to blood plasma
    • [Na+] is 150mM in plasma/ECF
  • Composition: cations
    • Na+(50mM)
    • K+ (4mM)
    • Ca2+ (1mM)
    • Mg2+ (1mM)
    • Cl (40mM)
    • Others (16mM)
  • Humidity: evaportation and convection less effective
    • When >75% evaporation, no longer physiologically effective
29
Q

What type of collagen predominates in the articular cartilage of synovial joints? What does this change to in osteoarthritis?

A

Type 2

Type 1

30
Q

Describe uric acid metabolism

A

Purines are broken down in the liver via xanthine oxidase into xanthines, then uric acid to then be excreted by the kidneys.

31
Q

Describe the formation of gouty crystals in the big toe in a patient with gout

A

Purines are broke down into uric acid. Excess uric acid in the blood combine with sodium (monosodiumurate), forms crystals which precipitate in joints (and the kidney)

32
Q

Why can’t you prescribe a thiazide diuretic to a pt with gout?

A

Thiazide dirutetics fx- inhibit Na+/Cl- co-transporter –> increased urine output

  • Also promote urate reabsorption in the PCT –> more urate in blood
33
Q

discuss the pharmacology and appropriate application of drugs used to treat gout

A
  • DECREASE PAIN AND SWELLING
    • NSAIDs
    • corticosteroids
    • colchicine (inhibits WBC migration)
  • Decrease uric acid
    • Decrease synthesis via xanthine oxidase inhibitor- allopurinol
    • Increase secretion - uricosuric medications
34
Q

discuss the pharmacology and appropriate application of drugs used to treat osteoarthritis

A
  • Pain relief- paracetamol, NSAIDs, opioids
    • PPIs (Often given with NSAIDs to prevent ulcers)
  • Stem Cell Treatment?
  • Intra-articular injections of hyaluronan or glucocorticoids.
  • Surgery (Knee replacement)
35
Q

discuss the pharmacology and appropriate application of drugs used to treat rheumatoid arthritis

A
  • hydrocortisones (decreases transcription of immune mediators)
  • TNF-alpha blockers
  • NSAIDs for pain management
  • consider protein pump inhibitor (PPI) to prevent stomach ulcers
36
Q

How does hydrocortisone affect bone formation/resorption?

A

Cortisol causes increased bone resorption through decreased OPG expressed and increasing RANKL expression in osteoblasts.

37
Q

How does oestrogen affect bone formation?

A
  • Increased osteoblasts activity
  • release TGF-B increase lifespan osteoblasts and apoptose osteoclasts
  • inhibits RANKL –> decreased osteoclast activation
38
Q

How does low serum [Ca2+] affect the bone and what hormone is involved?

A
  • Low [Ca2+] –> PTH release
  • PTH binds onto osteoblasts
    • Inhibition of osteoblast release of OPG which normally blocks the RANKL from the RANK receptor, so osteoclasts can’t bind to this cute hat
    • RANKL increased expression
    • Osteoblast proliferation
  • Without OPG, osteoclasts RANKL receptor bind to RANKL
    • Osteoclast proliferation
    • Differentiation into active macrophage fx
  • Osteoclasts also respond to M-CSF (macropahge colony stimulating factor) due to their macrophage like lineage
  • Release of HCl- onto bone –> bone resorption –> increased blood [Ca2+] [PO4-]
39
Q

Describe the 5 stages and timeframes involved in fracture healing

A

MD1 FBS (28 decks)

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