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2021 medicine > 4th May [22nd-30th] > Flashcards

4th May [22nd-30th] Flashcards

1
Q

Where is most calcium in the body stored?

A

99% in the bones as calcium phosphate

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2
Q

Breakdown of calcium in cells?

A

0.01% in cells, 0.99% in the extracellular spaces like the blood

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3
Q

What can high intercellular calcium cause?

A

Apoptosis

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4
Q

Where is the extracellular calcium found?

A

Diffusible

  • free-ionised: hormone secretion, muscle contraction, blood coagulation
  • complexed: calcium oxalate, electronically not neutral cellular prcoess

Non-diffusible
- albumin and calcium; too large to diffuse into cells

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5
Q

How are extracellular levels controlled?

A

Parathyroid cell detects change in level -> parathyroid hormone has various actions:

  1. Bones release calcium
  2. kidneys reabsorb calcium
  3. calcitriol [active vitamin D]-> GI absorbs calcium
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6
Q

How can acidosis cause symptoms of hyperacalcaemia?

A

Normally, parathyroid hcells keeps calcium between 8.5-10mg/dL.

However, albumin has nehative COOH groups and if increased H+ the COOH- groups pick up excess H+ and become positively charged -> positive albumin sand Ca2+ now repel each other -> more free-ionised Ca2+ [as less not diffusible] = Sx of hypercalcaemia

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7
Q

How can dehydration cause pseudocalcaemia? [rare]

A

In hyperalbuminaemia, more bound Ca2+ though some free-ionised Ca2+ as it is homronally regulated -> false hypercalaemia

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8
Q

Two main causes of true hypercalcaemia?

A

Osteoclastic bone resorption [most common]

Excess vitamin D

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9
Q

How do osteoclasts work?

A

Break down bone -> Ca2+ into the blood

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10
Q

Causes of osteoclast bone resorption

A
  • Can happen due to parathyroid glad overgrowth -> increased parathyroid hormone
  • Malignant tumours -> secrete parathyroid hormone related protein [PTHrP]
  • malignant turmours can also cause osteoclast death -> lytic bone lesions
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11
Q

How can excess vitamin D happen?

A

Diet, or through supplements
- increased absorption of Ca2+ in the gut
Medications like thiazide diuretics
- increased reabsorption distal tubule

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12
Q

Physiology of neurological Sx related to hypercalcaemia

A

Resting state of neurone stabilised by Ca2+ which prevents spontaneous depolarisation
In hypercalcaemia, sodium channels less liely to open
- harder to depolarise, less excitable
- slower/absent reflexes
- slow muscle contraction = constipation/general muscle weakness
- confusion/hallucinations/stupor in CNS

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13
Q

Neuro Sx of hypercalcaemia

A

Slow muscle contraction

  • constipation
  • generalised muscle weakness

CNS

  • confusion
  • hallucinations
  • stupor
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14
Q

Nephro physiology of hyeprcalcaemia

A

High Ca2+ excreted in urine -> hypercalciuria -> loss of fluid kidneys -> dehydrated
Combination of hypercalciuria+dehydration can lead to calcium oxalate kidney stones

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15
Q

Mnemonic for primary hyperparathyroidism [think also for hypercalcaemia]

A

Bones, stones, abdominal groans, psychic moans

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16
Q

Diagnosing hypercalcaemia

A 
Elevated Ca2+ in the blood [over 10.5mg/dL]
Electrocardiogram
- OSBORN wave
- short QT wave
- bradycardia
- AV block

Lab tests
- parathyroid, vitamin D, albumin, phosphorus, magnesium

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17
Q

Treating hypercalcaemia

A

lower calcium in the blood

  • increase urinary excretion with hydration [more Ca2+ filtered], loop diuretics [inhibit Ca2+ reabsorption]
  • increased GI excretion -> glucocorticoids -> decrease Ca2+ absorption
  • prevent bone resorption: bisphosphonates+calcium => inhibit osteoclasts
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18
Q

Treating acute hypercalcaemia [handbook]

A
  1. Correct dehydration [if dehydrated, give 0.9% saline]
  2. Bisphosphonates: prevent osteoclast activity. Single dose pamidronate lowers calcium over 2-3d, maximum effect at 1 week. Zoledronate acid usually single dose effective at 90mg.
  3. Further Mx: chemo to help malignancy, steroid used in sarcoidosis [eg prednisolone 40-60mg/d], salmon calcitonin acts similarly to bisphosphonates but now rarely used. Use of furosemide cententious helps Ca2+ renal excretion but cna worsen dehydration and so worsen hypercalcaemia. Should only be used once fully rehydrated. Avoid thiazides.
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19
Q

What is the haematocrit?

A

Ratio of RBC in the total blood volume

Normally, around 45%.

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20
Q

How common is the JAK2 mutation in PV?

A

90%

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21
Q

What produces erythropoietin?

A

Kindeys

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22
Q

How does erythropoietin work?

A
  • Activates the JAK2 gene
  • mutation keeps the JAK2 gene activated, even in the absence of erythropoeitin
  • becomes dominant haemopoeitic stem cell in bone marrow
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23
Q

How can PV lead to myelofibrosis?

A

As haemapoetin stem cells become dominant in the bone marrow, cells start to die out

  • this leads to scar tissue
  • BM can no longer produce RBCs -> decrease in RBCs/plts/WCC
  • known as spent phase in decreased RBC -? myleofibrosis
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24
Q

Sx of PV early stages

A 
fatigue
itching [esp. hot showeer due to increased eosinophils and basophils]
trouble breathing when you lie down
trouble concentrating
unplanned weight loss
pain in your abdomen
feeling easily full
blurred or double vision
dizziness
weakness
heavy sweating
bleeding or bruising
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25
Q

Sx of PV in later stages

A

As the disease progresses and your blood becomes thickened with more red blood cells, more serious symptoms can appear, such as:

heavy bleeding from even minor cuts
swollen joints
bone pain
reddish color to your face
bleeding gums
burning feeling in your hands or feet
splenomegaly
buildup of kidney stones
more prone to strokes/heart attacks/DVT/Budd-Chiari
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26
Q

Blood tests done for PV

A

Bloods

  • increased haemoglobin, increased haematocrit, increased WBC, increased plts
  • decreased erythropoeitin
  • BM biopsy for fibrosis
  • genetic test for JAK2 mutation
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27
Q

Tx for PV

A
  • Phlebotomy: can’t be used for donations, but can be used for autologous transplantation [such as in spent phase]
  • Myelosuppressive medication: hydroxyuria, ruxolitinib [JAK2 inhibitor]
  • antihistamines, apsirin etc.
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28
Q

Where do lymphoma cancers arise from?

A

Tumours derived from lymphocytes which are B cells or T cells

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29
Q

Broadly, what are lymphomas categorised into?

A

Hodgkins

Non-hodgkins

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30
Q

Main differences between HL and NHL

A

Hodgkins

  • arise from B cells generally
  • spread contiguously to nearby lymph nodes, rarely involving extra nodal sites
  • bimodal ages: 20s, and over 60s
  • Reed-Sternberg cells [owl eyes] B cells

NHL

  • B/T-cells
  • more common with 90% of cases [I think]
  • spreads non-contiguously and involved in extra-nodal sites like skin/brain/GI
  • prognosis worse
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31
Q

Compare B-cell to T- cell NHL

A

B-cell

  • more common
  • neoplastic B-cells express CD20
  • various types [growth rate]: 1. Follicular 2. Burkitt 3. Mantle cell 4. MZL
  • can be indolent, aggressive, highly aggressive

T-cell

  • less common
  • types include: 1. LPL 2. Adult T-cell 3. MF
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32
Q

Define myeloproliferative disorders

A

Group of cancers where there’s an excess of RBCs, WBCs, plts produced by the bone marrow

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33
Q

Main categories of myeloproliferative disorders [with accompanied mutations]

A
  1. CML - > Philadelphia chromsome [BCR-ABL]
  2. CNL -> CSF3R gene, excl. other cancers
  3. PV -> JAK2 mutation
  4. PMF -> JAK2, CALR, MPL
  5. ET -> 450x109/L plts
  6. Chronic eosinophilic leukemia -> PDGFR
  7. MPN, unclassifiable [MPN-U] -> Dx of exlcusion
  8. Mastocytosis
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34
Q

Common population myeloproliferative disorders found in?

A

Mainly the elderly

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35
Q

Which blood components are affected in myeloproliferative disorders?

A

RBCs, WBCs, plts are all affected, however one dominant in each disorder

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36
Q

How can myeloproliferative disorders lead to attacks of gout?

A

rapid cell turnover -> nucleus -> pruein metabolism -> increased uric acid -> precipitate attacks of gout

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37
Q

What can all myeloproliferative disorders progress onto?

A

Acute myeloid luekemia [secondary]

38
Q

Which mutation do PV, PMF and ET all share?

A

V617F mutation -> activation of JAK2 kinase

39
Q

How does JAK2 kinase work in myeloproliferative disorders?

A
  • JAK2 kinase stimulates erythropoietin and thrombopoeitin in receptors but not GM-CSF
  • So EPO and TPO decrease as negative feedback ensues
40
Q

What can a pluripotent haematopoeitic stem cell turn into? Disorder where this can go wrong?

A
  1. Myeloid stem cell
  2. Lymphoid stem cell

Disorder = PMF

41
Q

What can a myeloid stem cell turn into?

Disorders where they can go wrong?

A
  1. Pro-erythroblast -> erythrocyte [PV]
  2. Myelobalst -> basophil/neutrophil/eosinophil [CML]
  3. Monoblast -> monocyte
  4. Megakaryoblast -> megakaryocyte -> plts [ET]
42
Q

What can lymphoid stem cells turn into?

A
  1. B -cells
  2. T-cells
  3. natural killer cells
43
Q

How high are plts in ET?

A

over 450

44
Q

If patient is under 60 y/o, what would you tend to give them?

A

interferon-gamma

45
Q

Mutations in ET?

A

JAK2, CALR, MPL mutation

46
Q

Dx for ET

A

Platelet count

Also, exclusion to rule out CML, reactive causes, iron deficiency anaemia

47
Q

Ix for ET?

A

CRP/ESR for infection, blood count for platelet numbers, genetic testing, iron/ferritin, BCR-ABL for CML

48
Q

Tx for ET

A
  • hydroxycarbamide, inteferon gamma, anagrelide can reduce platelets
  • aspirin
  • plateletpharesis -> if platelets are very high
49
Q

Sx of CML

A

Splenomegaly, increased WCC, fatigue

50
Q

Main Ix for CML

A

BCR-ABL

51
Q

Which stage are most patients diagnosed with CML?

A

Asymptomatic stage

52
Q

What symptom may upper quadrant pain signify in a patient with CML?

A

Splenomegaly

53
Q

What is the main Tx for CML?

A

Tyrosine kinase inhibitors

- dasasatinib, netoinib

54
Q

What is the first-line for myelpfibrosis?

A

Imitinib

55
Q

What is cholesterol embolisiton?

A

Ruptured atherosclerotic plaque from a large artery

56
Q

How is the M-spike created in myeloma?

A

1 cancerous cell proliferates and produces lots of monoclonal antibodies

57
Q

How can the light chains of antibodies be divided?

A

Into kappa and lambda regions

58
Q

in an infection, how do the light chains in antibodies repsond?

A

equal ratio of lambda and kappa

59
Q

in myeloma, how do light chain antibodies respond?

A

unequal ratio [over 1] of kappa and lambda

60
Q

How is myeloma commonly diagnosed?

A

Eletectrophoresis looking at the number of antibodies and comparing it to albumin
Comparing kappa and lambda regions on the antibody light chains.

61
Q

What does MGUS stand for?

A

Monoclonal gammopathy of undetermined singificance

62
Q

Mnemonic for pancreatitis?

A 
I - idiopathic
G - gallstones
E - ethanol
T - trauma
S - steroids
M - mumps/malignancy
A - autoimmune
S - scorpion
H - hyperglycerides/hypercalcaemia
E - ERCP [post]
D - drugs [azathioprine, pentamidine, bactrim]
63
Q

Which blood disorder can menstruating women suffer from?

A

Menstruating women x6 more likely to get iron deficiency anaemia

64
Q

Causes of low platelets

A
  1. Failure of central production
    - leukemia
    - dysplasia
    - AA
  2. Peripheral consumption
    - DIC
    - ITP
    - sepsis
    - HIT
    - TTP
    - ITP [generate platlets to own antibodies]
65
Q

What is ITP?

A

Immune thrombocytopenic purpura (ITP), also known as idiopathic thrombocytopenic purpura or immune thrombocytopenia, is a type of thrombocytopenic purpura defined as an isolated low platelet count with a normal bone marrow in the absence of other causes of low platelets.[1] It causes a characteristic red or purple bruise-like rash and an increased tendency to bleed. Two distinct clinical syndromes manifest as an acute condition in children and a chronic condition in adults. The acute form often follows an infection and spontaneously resolves within two months. Chronic immune thrombocytopenia persists longer than six months with a specific cause being unknown.

ITP is an autoimmune disease with antibodies detectable against several platelet surface structures.

66
Q

What is TTP?

A

Thrombotic thrombocytopenic purpura (TTP) is a blood disorder that results in blood clots forming in small blood vessels throughout the body.[2] This results in a low platelet count, low red blood cells due to their breakdown, and often kidney, heart, and brain dysfunction.[1] Symptoms may include large bruises, fever, weakness, shortness of breath, confusion, and headache.[2][3] Repeated episodes may occur.[3]

67
Q

What is melphalan?

A

Alkylating agent used against myeloma
Nitrogen bases and used as mustard gas in WW1
Works by interfering with creation of DNA/RNA

68
Q

DVD drug therapy

A

Darzalex, velcade and dexamethasone

69
Q

Type of cancer is multiple myeloma?

A

B cell cancer [plasma cells]

70
Q

Sx of MM?

A

Often no Sx initially -> bone pain, anaemia, kidney dysfunction develops

71
Q

What is the condition which MM often originate from?

A

MGUS

72
Q

CRAB mnemonic for MM

A

C: calcium over 2.75mmol/l
R: renal creatinine over 40
A: anaemia over 10g/dl
B: bone lesions on radiography

73
Q

How common is bone pain?

A

In 70% of patients it’s present

74
Q

Type of anaemia in MM?

A

Normocytic

75
Q

Neuro symptoms of MM

A

Hypercalcaemia

  • weakness
  • confusion
  • fatigue

Hyper-viscosity

  • headache
  • vision
  • retinopathy

Neuropathy

  • radicular pain
  • bowel
  • bladder
  • carpal tunnel
  • peripheral neuropathy may occur with Tx for MM
76
Q

RFs for MM

A

MGUS
Obesity
FHx
EBV [particularly those with immunodeficiency]

77
Q

Dx for MM

A 
Protein electrophoresis of the blood/urine which might show M bands
IgG most common, then IgA/IgM
IgD and E rare
Raised calcium and creatinine
Biopsy
78
Q

Criteria for Dx of MM

A
  1. Clonal plasma cells above 10%
  2. Monoclonal protein over 3g/dL
  3. Evidence of end-organ damage in CRAB
79
Q

Chemotherapy drug classes

A
  1. Thalidomide
  2. Steroid
  3. Monoclonal
  4. Protease inhibitor [-nib]
  5. Alkylating agents
80
Q

Define thrombocytopenia

A

Platelet count under 150,000/mm3

81
Q

What are platelets made by?

A

Megakaryocytes

82
Q

How many platelets does each megakaryocyte mkae?

A

1-5k

83
Q

Normal physiology of a blood clot

A
  1. Vasoconstriction [platelet/wWF]
  2. Platelet plug [adhesion onto exposed collagen, activation, aggregation]
  3. Coagulation [clotting factor activation causes prothrombin to thrombin etc.]
84
Q

What is platelet production stimulated by?q

A

Thrombopoeitin and inflammation from cytokines like IL-6

85
Q

How many platelets are sequestered in the spleen at any one time?

A

1/3rd

86
Q

How long do platelets live for?

A

about 7d

87
Q

How are platelets removed in the body?

A

Platelets removed by monocytes of the reticuloendothelaial system [i.e. liver/spleen]

88
Q

Causes of thrombocytopenia

A
  1. Reduced platelet production: bone marrow disroders [like failure, acute leukemia, malignancy, alcohol whihc can all lead to disruption in thrombopoeisis], ITP
  2. Increased platelet consumption: DIC, TTP/HUS, HIT
  3. Splenomegaly: portal hypertension, Felty’s syndrome [such as seen in RA]
  4. Dilatational: massive fluid resuscitation
  5. Increased platelet destruction: ITP [when antibodies attack platelets]

Infection common cause which can lead to many different causes of thrombocytopenia

89
Q

Skin Sx of thrombocytopenia

A

Purpura, petechia

90
Q

Other Sx of thrombocytopenia

A

Mucosal bleeding, lymphadenopathy, splenomegaly/hepatomegaly, fever, loss of appetite

2021 medicine (10 decks)

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