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EMS - JL > 26,27,28 > Flashcards

26,27,28 Flashcards

1
Q

Why do we get metabolic acidosis

A

Increased H+ formation
Acid ingestion
Reduced renal H+ Excretion
Loss of bicarbonate

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2
Q

H+, pCO2 and pO2 in metabolic acidosis

A

High H+ and pO2

Low CO2

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3
Q

Why do we get metabolic alkalosis?

A

Generation of bicarbonate by gastric mucosa
Renal generation of HCO3- in hypokalaemia
Administration of bicarbonate

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4
Q

H+, pCO2 and pO2 in metabolic alkalosis

A

Low H+ and pO2

High CO2

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5
Q

Consequences of metabolic alkalosis

A

K+ goes into cell and urine
PO4 goes into cells
Get respiratory suppression

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6
Q

Causes of respiratory acidosis

A

CO2 retention due to:

a) Inadequate ventilation
b) Parenchymal lung disease
c) Inadequate perfusion

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7
Q

H+, pCO2 and pO2 in respiratory acidosis

A

H+ and CO2 High

pO2 low

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8
Q

Cause of respiratory alkalosis

A

Increased CO2 excretion due to excessive ventilation producing alkalosis (e.g. fast heavy breathing)

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9
Q

H+, pCO2 and pO2 in respiratory alkalosis

A

Low H+ and low CO2

High pO2

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10
Q

Why do we get increased H+ formation

A

Ketoacidosis, diabetic or alcoholic
Lactic acidosis
Poisoning
Inherited organic acidoses

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11
Q

When would we suspect metabolic acidosis

A

Tiredness and weight loss

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12
Q

What happens in keto-acidosis

A

Hyperglycaemia
Osmotix diuresis - due to pre-renal uraemia
Hyperketonaemia
Increased FFA

ALL of these lead to acidosis

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13
Q

Two types of lactic acidosis

A

Type a - shock

Type b - metabolic and toxic causes

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14
Q

Why do we get acidosis in an alcoholic

A

NAD+ depletino (thiamine)
Thiamine deficiency (which is a pyruvate dehydrogenase Co-factor, hence without it can’t make acetyl-CoA)
Enhanced glycolysis for ATP formation
FFA Made into acetyl-coA which then also produces ketones
Keto-acids secondary to counter-regulatory hormones
Get profuse vommiting

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15
Q

How does high lactate = lactic acidosis

A

In alkalosis: Increased glycolysis, reduced oxygen delivery due to shift in oxygen dissociation curve, lactate induced vasoconstriction, impaired mitochondrial respiration

OR Oxygen debt due to further anaerobic lactate production causing hyperventilation

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16
Q

What causes reduced H+ Excretion

A

Renal tubular acidosis

Generalised renal failure

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17
Q

What happens in renal failure

A

Reduced volume of nephrons
Increased bicarbonate loss, reduced NH4+ excretion
NH4+ to liver for urea + H+ synthesis
Only fraction of NH4+ derived from glutamine (normally approx 100%)

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18
Q

How much co2 do we produce daily

A

25mol/day

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19
Q

how much unmetabolised acid do we produce a day

A

50mmol/day

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20
Q

What is normal plasma concentration of acid

A

40nmol/L

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21
Q

What are the buffering systems

A 
Haemoglobin
Bicarbonate
Phosphate
Protein
Ammonia
Organic acids

Only Hb and bicarbonate are of real important

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22
Q

What is normal blood pH

A

7.35 to 7.45

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23
Q

What are the sites for acid base metabolism

A

Lungs, kidneys, liver, GI

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24
Q

What happens in tissue gas exchange with CO2

A

Co2 non-polar diffuses into cell
Forms HCO3- and H+
H+ binds with HbO2
Forms H+HB and releases O2 from the cell

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25
Q

What causes a right shift in the oxygen dissociation curve

A

Increased temperature
Increased 2,3-DPG
Decreased pH (acidosis)

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26
Q

What happens in renal reclamation of bicarbonate

A

HCO3- is small so gets lost by the kidneys
Na+/H+ pump, pumps Na+ out of the kidney and H+ in
H+ binds with HCO3- –> forms H2) and CO2
CO2 reabsorbed and reforms HCO3-

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27
Q

Renal Regeneration of bicarbonate

A

Glutamine converted to NH3 and NH4+
NH4+ then excreted –> allows us to excrete more H+

Also HPO4 can be turned into H2PO4- allowing us to remove more H+

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28
Q

Where do mineral corticoids (aldosterone) act on the kindey

A

Distal tubule

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29
Q

What happens if alkalotic in the distal tubule

A

K+ lost, H+ retained

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30
Q

What happens if acidotic in the distal tubule

A

K+ retained H+ lost

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31
Q

Discuss acid/base balance in the GI tract

A

Stomach excretes acid for digestion

Pancreatic juice contains HCO3- to neutralise the stomach acid

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32
Q

Where is the dominant site for lactate production

A

The liver

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33
Q

Where is the only site of urea synthesis

A

The liver

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34
Q

Is acid-base disorders due to the liver common

A

No as the liver has such an excess capacity for dealing with it

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35
Q

What are protein and amino acids broken down into

A

Carbon skeleton and NH4+

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36
Q

What is stimulated by alkalosis

A

NH4+ to NH3 to be lost in the urine

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37
Q

What is inhibited by acidosis

A

the formatin of H+ and urea

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38
Q

What happens in sever liver failure

A

Metabolic acidosis
NH4+ toxicity as:

NH4+ and oxo-glutamate can’t be made into glutamine
and

NH4+ and CO2 can’t be made into urea and H+

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39
Q

why do cells need to adapt

A

due to changes in the environment or the demand

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40
Q

Which cells don’t need to adapt

A

Fibroblasts - survive severe metabolic stress without harm e.g. oxygen absence

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41
Q

Which cells adapt easily

A

Epithelial cells
Lable cell population that can adapt easily with an active stem cell population

Highly adaptive

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42
Q

Which cells do not adapt easily

A

Cerebral neurons

Permanent cell population - terminally differentiated, highly specialised and easily damage

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43
Q

What is physiological adaptation

A

Response to normal changes

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44
Q

What is pathological adaptation

A

Response to disease related changes

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45
Q

What happens in hypertrophy

A

Increased size of existing cells, increased functional capacity, increased synthesis of structural components, increased metabolism

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46
Q

Where does hypertrophy particularly occur

A

In cardiac and skeletal muscle

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47
Q

Physiological hypertrophy

A

Utero in pregancy

Marathon runners

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48
Q

Pathological hypertrophy

A

LV hypertrophy, aortic stenosis, urinary bladder with adenymyotamous hyperplasia of prostate

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49
Q

How to diagnose LV Hypertrophy

A

Clinical examination, ECG and imaging

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50
Q

Consequences of LV hypertrophy

A

Ventricular tachycardia, can be so large it can be functionally ischamic

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51
Q

What is subcelular hypertrophy and hyperplasia

A

Increase in size and number of sub cellular organelles

e.g. hepatocytes due to barbituates (increased P450 enzymes)

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52
Q

What cell populations does hyperplasia occur in

A

Lable and stable

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53
Q

Physiological hyperplasia

A

Hormonal

Compensatory (particularly kidneys if one is small)

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54
Q

Pathological hyperplasia

A

Excess hormones or growth factors

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55
Q

Describe gynocomastia

A

Increase in male breast size due to increased oestrogen (hyperplasia)

Can be pathological or physiological

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56
Q

What is graves disease

A

Auto-antibody to TSH receptor

Causes hyperplasia with an enlarged pale thyroid

57
Q

What is adenymomoatous hyperplasia of the prostate

A

Hyperplasia of the the prostate which occurs normally as age related

58
Q

What are hyper plastic nodleuls in the liver

A

When liver cells try to return back to normal but function is never fully restored

59
Q

What is atrophy

A

Reduction in cell size and number

60
Q

Physiological atrophy examples

A

Embryogenesis, uterus after pregnancy, menopause (decreased oestrogen decreases the size of the uterus)

61
Q

Pathological atrophy examples

A

Deceased work load, loss of innervation, inadequeate nutrition/blood supply/endocrine stimulation
Pressure

62
Q

What happens in renal artery stenosis

A

One kidney atrophies due to reduced blood flow

63
Q

What is hydronephrosis

A

Increased pressure in kidney due to obstructed bladder outflow causes atrophy

64
Q

Describe physiological atrophy in the thymus

A

Very big in child but replaced by fat in the adults

65
Q

What is sub cellular atrophy

A

Reduction in the volume of specific cells

66
Q

What is involution

A

Physiological atrophy by apoptosis (requires energy)

67
Q

What is brown pigment

A

Non-digestible part of the cell membrane

68
Q

What is ageneis

A

failure of formation of embryonic cell mass

69
Q

What is aplasia

A

failure of differentiation into organ specific tissue

70
Q

what is dysgenesis

A

failure of structural organisation of tissue into organs

71
Q

what is hypoplasia

A

Failure of growth of organ to full size

72
Q

Developmental causes of reduced cell mass

A

Agenesis
Aplasia
Dysgenesis
Hypoplasia

73
Q

What is significant about dysplasia

A

Earliest morphological manifestation of multistage neoplasia (irreversible)

Want to try and spot before it invades the basement membrane

74
Q

What is metaplasia

A

the transformation of one cell type to another caused by the transdifferentiation of stem cells

75
Q

Epithelium in vagina

A

straified squamous

76
Q

epihtleium in endocervix

A

squamocolumnar

77
Q

Describe metaplasia in cervix

A

In puberty increased oestrogen causes stromal bulk of cervix

The squamocolumnar junction moves into the vagina (cervical ectopic)

Columnar epithelium becomes squamous (squamous metaplasia) due to the acidic vaginal environment

78
Q

Where does HPV cause cervical cancer

A

Squamocolumnar junction

79
Q

What happens to the squamocolumnar junction in menopaure

A

THE Squamocolumnar junction moves back up the cervix but no metaplasia occurs

Makes screening less effective as the SCJ is in the cervical canal so can’t swab it but cervical cancer is likely to occur here

80
Q

Pathological metaplasia in the bronci

A

Smoking causes change from pseudo stratified ciliated to squamous

81
Q

Pathological metaplasia in bladder urothelium

A

Urothelium changes to squamous due schistosomiasis, long standing catheter and bladder calculous

82
Q

Pathological metaplasia in fibrocollagenous tissu

A

Changes to bone due to chronic trauma

83
Q

Pathological metaplasia oesophagus

A

Changes from squamous to columnar due to acid reflux

This is barretts oesophagus - predisposes us to adenomas carcinoma

84
Q

What is squamous metaplasia in the cervix linked to

A

CIN and squamous cell carcinoma

85
Q

What is endometrial hyperplasia due to increased oestrogen linked to

A

Adenocarcinomas

Common due to obesity as fat cells produce oestrogen

86
Q

What is parathyroid hyperplasia linked to

A

Chronic renal failure due to adenoma

87
Q

What is squamous metaplasia in bronchi linked to

A

Dysplasia and squamous cell carcinoma

88
Q

What is squamous metaplasia in the bladder linked to

A

squamous cell carcinoma

89
Q

what is glandular metaplasia in the oesophagus linked to

A

adenocarcinoma

90
Q

What is a neoplasm

A

a lesion resulting from the autonomous growth of cells that persist in the absence of the initiating stimulus

91
Q

cancer from epithelial cells

A

carcinoma

92
Q

cancer from connective tissue

A

sarcoma

93
Q

cancer from lymphoid or haematopoietic organs

A

lymphomas/leukaemias

94
Q

Commonest cancer for mortality

A

lung cancer

95
Q

4 main characteristics of tumours

A

Differentiation
Rate of growth - malignant tumours tend to grow more rapidly
local invasion
metastasis

96
Q

What is differentiation

A

the extent that neoplastic cells resemble the corresponding normal parenchymal cells, morphologically and functionally

97
Q

How differentiated are benign tummours

A

usually well -differentiated

mitoses rare

98
Q

how differentiated are malignant tumours

A

Wide range of differentiation

most exhibit morphological alterations showing malignant nature

99
Q

What is anaplasia

A

Poorly differntiated cells in a neoplasm
Do not resemble original cells
likely to be malignant

100
Q

What is pleomorphism

A

Variations in size and shape

101
Q

What is abnormal nuclear morphology

A

I.e. nuclei too large (normally want a 1:4/1:6 ratio to cytoplasm)
Irregular shape/pattern
Chormosome coarsely clumped along cell membrane (in more malignant tumours)
Hyper chromatin - dark colour

102
Q

What are mitoses

A

Indicative of high proliferation
Seen in hyperplasia and cells with high turnovers
Can see trip, quad or multipolar spindles in malignancy

103
Q

What is loss of polarity

A

When the cells orientation is disturbed (normally the nucleus is at the bottom of the cell)
Disorganised growth

104
Q

Grading of differentiation

A 
1 = well differentiated
3= poorly differntiated

Indicative of prognosis

105
Q

What do some tumours express not normally seen in adults

A

Some tumours express foetal proteins

106
Q

What happens in bronchogenic carcinoma

A

Corticotropin
Parathyroid like hormones
Insulin
Glucagon

107
Q

Benign tumours local invasion

A

Adhesive expansile masses
Localised to the site of origin
No capacity to infiltrate, invade or metastasise

108
Q

What can surround benign tumours

A

Encapsulation
ECM deposited by stromal cells - activated by hypoxia and from pressure of tumours

Forms a rim around the tumours formed of fibrous tissue

109
Q

What can surround malignant tumours

A

Pseudoencapsulation
Usually slow-growing
Microscopically rows of cells are penetrating the margin in a crab-like fashion

110
Q

Do malignant tumours respect anatomical boundaries?

A

No
Most penetrate organ surfaces and skin
Surgical resection difference as requires resection of adjacent normal tissue too

111
Q

What is metastasis

A

Spread of tumour to sites physically discontinuous with the primary tumour

Generally in malignant

112
Q

What is metastasis associated with

A

Lack of differentiation
Local invasion
Rapid growth
Large size

113
Q

Pathways of metastasis

A

Direct
Lymphatic
Haematgenous

114
Q

How does direct seeding occur

A

Neoplasm penetrates natural open field without physical barriers e.g. peritoneal cavity

BUT can remain confined to surface of peritoneal structures without penetrating e.g. pseudomyxoma peritoneal

115
Q

What is the most common pathway of seeding

A

Lymphatic spread

116
Q

Do tumours have lymphatic channels

A

NO - lymph vessels are at the tumour margin

Pattern of lymph node involvement follows the route of lymph drainage

117
Q

Where do breast cancers present lymphatically

A

Presents in the upper outer quadrant
Affects axillae node first
Then infra and supra clavicular nodes become involved

118
Q

Significance of axillary node in breast cancer

A

First site of spread of breast cancer

Determination of axillary node status determines future course of disease and what therapy is most suitable

119
Q

What is the sentinel node

A

The first node in regional lymphatic basin that receives lymph flow from the primary tumour

120
Q

How do we identify sentinel node

A

Inject radioactivelly labelled dyes

Frozen section during surgery can lead/guide surgeon to appropriate therapy

121
Q

Are regional barriers good at preventing further tumour dissemination

A

Usually they are effective

Cells arrest within node - can be destroyed by a tumour specific immune response

122
Q

Do all enlarged nodes have cancer in?

A

No - drainage of tumour cell debris and tumour antigens can cause reactive change in nodes

123
Q

What is haematogenous spread typical of

A

Sarcomas

BUT not strictly confined to this method

124
Q

What is lymphatic spread typical of?

A

carcinoma

BUT not strictly confined to this method

125
Q

What vessels are more easily penetrated by cancer

A

Veins due to their thinner walls

Blood borne cells then follow the venous flow draining the site of the neoplasm

126
Q

Where do metastasis via haematogenous spread usually come to a rest

A

In the first encountered capillary bed

Commonly Liver (portal circulation)
Lungs (caval) most
127
Q

What are the most frequent sites of haematgeonous spread to

A

Liver (portal)

Lungs (caval)

128
Q

What is stroma

A

The connective tissue framework that neoplastic cells are embedded in

Provides mechanical support, intercellular signalling, nutrition

129
Q

What is a desmoplastic reaction

A

Fibrous stroma formation due to induction of connective tissue proliferation by growth factors from the tumour cells

130
Q

Clinical complications of tumours

A

Compression
Destruction
Metabolic

131
Q

Non specific metabolic effects of tumours

A 
Cachexia
Wardburg effect
Neuropathies
Myopathies
Venous thrombosis
132
Q

Compression complications of tumours

A

Displacement of adjacent tumours

I.e. benign pituitary tumours can compress the pituitary gland obliteration the function causing hypopituitarism

133
Q

Destruction complications of tumours

A

Invasion - rapidly fatal if it invades vital structures e.g. arteries
Or mucosal surfaces invaded causeing ulceration e.g. GI leading to anaemia

134
Q

Metabolic complications of tumours

A

Well differentiated tumours can retain functional propertios

But thyrotoxicosis in thyroid adenoma

135
Q

Inappropriate metabolic response in tumours

A

Called paraneoplastic

I.e. ACTH/ADH in small cell lung cancer

136
Q

What is the wardburg effect

A

Produces energy by high rate of glycolysis with fermentation of lactic acid

137
Q

How do we detect the ward burg fefect

A

Used in imaging PET scanning (FDG Uptake)

138
Q

Summary of benign tumours

A

Well differentiated
Slow rate of growth
No local invasion
No metastasis

139
Q

Summary of malignant tumours

A

Variable differentiation
Fast rate of growth
Local invasion
Metastasis

EMS - JL (10 decks)

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