Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Year 5 😊✌🏼 > Path > Flashcards

Path Flashcards

1
Q

Where is cholesterol in the intetstine from?

A
  • diet
  • bile duct
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How is cholesterol in the intestine solubilised?

A

in mixed micelles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where are bile acids reabsorbed?

A

terminal ileum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What effect does cholesterol have on HMG-CoA-reductase?

A

it inhibits the enzyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

fates of cholesterol in the liver

A
  • hydrolysed via 7-alpha-hydroxylase into Bile Acids, released via bile ducts (major determinants of cholesterol absorbtion)
  • esterified via ACAT to cholesterol ester; incorporated with triglyceride and apoB into VLDLs with transfer protein MTP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How are triglycerides moved from small intestine to plasma?

A

via chylomicrons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How is LDL taken up by cells?

A
  • binds to LDL R
  • coated pits
  • invagination

processed by lysosomes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How common is homozygous and heterozygous familial hypercholesterolaemia?

A

homozygous: 1 in 10^6

heterozygous: 1 in 500

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is PCSK9? What happens in gain and loss of function mutations?

A

a chaperone protein

its role is to bind to the LDL receptor and promote its degradation

gain of function mutations -> high LDL (because more LDL R is degraded and LDL not taken up by liver)
loss of function mutations -> low LDL

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What medications are used to lower cholesterol? What effects do they have on HDL, LDL and TG?

A

statins - good reduction in LDL, slight reduction of TG, slight elevation of HDL

fibrates - very good at lowering TG, slight reduction/increase in LDL/HDL

resins - bind bile acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Pharmacological approaches to obesity

A

orlistat - inhibits pancreatic lipase -> not hydrolysed, not absorbed, excreted via stool

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

surgical approaches to obesity (and indication)

A

bariatric surgery

if BMI >40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Different types of bariatric surgery

A
  • gastric binding
  • roux-en-Y bypass
  • biliopancreatic diversion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Why can people with sarcioud have high Ca?

A

1-a-hydroxylase can be expressed lungs; uncontrolled; activation of vitamin D -> high CA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

25-hydroxylase is found where?

A

Liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Where is 1-alpha-hydroxylase found?

A

KIDNEYS

can be ectopiicallly expressed in sarcoid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

When do you prescribe cholecalciferol and calcitriol?

A

calcitriol is dangerous because it is active Vit D3; only prescribed in renal failure; easy to overdose;

cholecalciferol - OTC, has to be activated;

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Compare osteoporosis vs osteomalacia

A

Osteoporosis: reduced bone density with normal biochemistry

Osteomalacia: bone demineralisation; Blood: low Ca, low phos, high ALP/PTH?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

How do you calculate corrected calcium?

A

CC = measured calcium + 0.02x(40-albumin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

T-score vs Z-score

A

T-score SD of 20yo
Z-score is SD from age-matched

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Causes of osteoporosis

A
  • childhood illness
  • menopause
  • corticosteroid therapy
  • lifestyle: sedentary, EtOH, smoking, low BMI/nutritional
  • endocrine: hyperprolactinaemia, thyrotoxicosis, Cushing’s
  • other e.g. genetic, prolonged intercurrent illness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Mx of osteoporisis

A

lifestyle: weight bearing exercise, stop smoking, reduce etoh

Drugs
- vit D / Ca
- bisphosphonates (e.g. alendronate) -> decreased bone resorption -> very strong bone, not biodegradable; unnatural phosphate; osteoblasts Can use it, casts struggle with breakdown. do not have it with calcium, taken 1x/w on empty sttomach with water and nothing else. gut irritant.
alternative is 1/year IV zonlendronate
- teriparatide (PTH) derivative - anabolc;
- Strontium: anabolic + anti-respoptive
- oestrogens/HRT
- SERMs e.g, raloxifene (

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Tamoxifen actions

A

Tamoxifen agonist in bone, antagonist in breast

raloxifene similar; good for bone and prevent Br ca but worsen Sx of menopause.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Which antibiotic groups belong to beta lactams?

A

Penicllins
Cephalosporins
Carbopenems
Monobactams

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Examples og glycopeptide abx

A

teicoplanin
vancomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

glycopeptides - what bacteria do they work against?

A

gram +ve only

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Abx for C diff

A

Vancomycin (ora)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Can you give tetracycline to children and pregnant women?

A

No!

teratogenic and deposit in growing bones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Main risk of chloramphenicol

A

aplastic anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Drug interaction of linezolid

A

interferes with SSRIs, can cause serotonin syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Commonest cause of inborn errors of immunity

A
  1. antibody deficiency
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Clinical features of immune deficiencies

A
  • susceptibility to infection
  • AID
  • allergic diseases
  • autoinflammatory disease
  • viral related cancers (EBV, HPV)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What age group is mainly affected by PID?

A

children > adults

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Examples of primary immune deficiencies

A

SCID

XLA

CGD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q
A

• Severe (sepsis, need for intravenous antibiotics or fungal drugs)

• Persistent ( Multiple course of antibiotics to treat standard bacterial chest or
sinus infection)

• Unusual infections (Opportunistic organism (Pneumocystis jirovecci, CMV, Live vaccine induced infection))

• Recurrent (More than 2 episodes of pneumonia within a year • More than 8 episodes of Otitis Media in a child)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Management of CGD

A

Cotrimoxazole and itraconazole prophylaxis
Adjunctive IFN-gamma, Stem cell and gene therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

treatment of SCID

A

Stem cell transplant

?gene therapy (complicated by T-cell leukemia in 20%; T-cell function restored but not B-cells restored)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Life expectancy of patients with infection phenotype CVID

A

normal with IgG replacement therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

causes of raised RBC count

A

Primary; polycythaemia vera

secondary: high altitude

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Leukoerythroblastic anaemia - what is it? what does it indicate?

A
  • variable degree of anaemia
  • specific morphological features in the blood film (tear drop RBCs, nucleated RBCs, myelocytes)

indicates abnormal bone marrow infiltration (malignancy (leukaemia, lymphoma, myeloma; metastasis to bone; ), severe infection (rarely), myelofbrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

causes of reactive neutrophiilia

A
  • PYOGENIC INFECTION
  • corticosteroids
  • underlying neoplasia
  • tissue inflammation (e.g.colitis, pancreatitis myocarditis or MI)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

causes for reactive eosinophlia

A

Parasitic infestation
Allergic diseases e.g. asthma, rheumatoid, polyarteritis, pulmonary eosinophilia.
Neoplasms, esp. Hodgkin’s, T-cell NHL (reactive eosinophilia)
Drugs (reaction erythema multiforme)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Causes for monocytosis

A

TB, brucella, typhoid
Viral; CMV, varicella zoster
sarcoidosis
chronic myelomonocytic leukaemia (MDS)

rare but seen in certain chronic infections and primary haematological disorders

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

causes for lymphocytosis

A

EBV, CMV, Toxoplasma (Infectious mononucleosis IM)
infectious hepatitis, rubella, herpes infections
autoimmune disorders
Sarcoidosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

causes for lymphopenia?

A

Infection HIV
Auto immune disorders
Inherited immune deficiency syndromes
Drugs (chemotherapy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Triple assessment for Breast lump

A

Physical examination.
Imaging- Sonography, mammography & MRI
Pathology (cytopathology and/or histopathology).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Breast Cytopathology classification with definitions

A

C1 = inadequate
C2 = benign
C3 = atypia, probably benign
C4 = suspicious of malignancy
C5 = malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Breast history biopsy method

A

16-14 gauge needles (sometime 8-11 g)

US-guided or using stereographic techniques

with larger needles use vacuum assisted technologies, gives you more tissues.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Histology results in breast (classification and definition)

A

B1:normal tissue / inadequate sample
B2:benign lesion
B3:uncertain malignant potential
B4:suspicious of malignancy
B5:malignant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Duct ectasia

A

Inflammatory breast disease

5th -6th decade, multiparous women
Inflammation and dilation of large breast ducts.
Aetiology unclear.
Usually presents with nipple discharge.
Sometimes causes breast pain, breast mass and nipple retraction.
Cytology of nipple discharge shows proteinaceous material and inflammatory cells only.
Benign condition with no increased risk of malignancy.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Duct ectasia histology

A

Dilated duct
proteinaceous secretions
Periductal and interstitial inflammation – granulomatous
surround by inflammatory cells and macrophages

52
Q

Acute mastitis

A

Acute inflammation in the breast.

Often seen in lactating women due to cracked skin and stasis of milk.

May also complicate duct ectasia.

Staphylococci the usual organism.

Presents with a painful red breast.

Drainage & antibiotics usually curative.

53
Q

(Breast) fat necrosis

A

An inflammatory reaction to damaged adipose tissue.

Caused by trauma, surgery, radiotherapy.

Presents with a breast mass, late stages may show focal calcification.

Benign condition.

54
Q

Galactocoele

A

Cystic dilation of a duct during lactation

Usually multiple ducts

Tender palpable nodules

Secondary infection may convert these to acute mastitis or abscess

55
Q

Fibrocystic disease

A

A group of alterations in the breast which reflect normal, albeit exaggerated, responses to hormonal influences.

Very common.

Presents with breast lumpiness.

No increased risk for subsequent breast carcinoma.

56
Q

Fibrocystic disease on histology

A
  • fibrosis (replaces normal storma)
  • cystic
  • associated with adenoss/proliferaton of the gland

Three components, As the name indicates – Fibro – loose stroma is replaced by compressed fibrous tissue containing Cysts lined by flattened (larger cysts) to low cuboidal epithelium (smaller cysts) and adenosis – increased number of acini

Non proliferative changes – no usual type hyperplasia.

57
Q

Fibroadenoma

A

A benign neoplasm composed of fibrous and glandular tissue.

Common.

Presents as a circumscribed mobile breast lump in young women aged 20-30.

Simple “shelling out” curative.

58
Q

Phyllodes tumour

A

A group of potentially aggressive fibroepithelial neoplasms of the breast.

Uncommon tumours.

Present as enlarging masses in women aged over 50.

Some may arise within pre-existing fibroadenomas.

Vast majority behave in a benign fashion, but a small proportion can behave more aggressively.

59
Q

Intraductal papilloma

A

A benign papillary tumour arising within the duct system of the breast.

Arise within small terminal ductules (peripheral papillomas) or larger lactiferous ducts (central papillomas).

Common.

Seen mostly in women aged 40-60.

Central papillomas present with nipple discharge.
Peripheral papillomas may remain clinically silent if small.

Excision of involved duct is curative.

60
Q

Radial scar

A

A benign sclerosing lesion characterised by a central zone of scarring surrounded by a radiating zone of proliferating glandular tissue.

Range in size from tiny microscopic lesions to large clinically apparent masses.

Lesions >1 cm are sometimes called “complex sclerosing lesions”.

Reasonably common lesions.

Thought to represent an exuberant reparative phenomenon in response to areas of tissue damage in the breast.

Usually present as stellate masses on screening mammograms which may closely a carcinoma.

Excision is curative.

61
Q

Lifetime risk of breast cancer with BRCA mutation

A

up to 85%

62
Q

components of breast histological grading

A

1) tubule formation
2) nuclear pleomorphism
3)mitotic activity.

each given 1-3 points -> added up

3-5 points = grade 1 (well differentiated).
6-7 points = grade 2 (moderately differentiated).
8-9 points = grade 3 (poorly differentiated).

63
Q

Receptor status of low, high grade and basal like tumours of the breast

A
  • Low grade tumours tend to be ER/PR positive and Her2 negative.
  • High grade tumours tend to be ER/PR negative and Her2 positive.
  • Basal-like carcinomas are often ER/PR/Her2 negative (“triple negative”).
64
Q

Most important prognostic factor in breast tumours

A

The single most important prognostic factor is the status of the axillary lymph nodes.

Other important factors include tumour size, histological type, and histological grade.

65
Q

Women age for NHS Breast screening and programme

A

Women aged 47-73 are invited for screening every three years / 50-70 at the moment

66
Q

B5a vs B5b core biopsy result (breast)

A

B5a: DCIS

B5b: invasive carcinoma

67
Q

Most common disease of the male breast

A

Gynaecomastia

68
Q

Gynaecomastia

A

Refers to enlargement of the male breast.
Pubertal boys and older men aged over 50.
Idiopathic or associated with drugs (both therapeutic and recreational).
Histologically the breast ducts show epithelial hyperplasia with typical finger-like projections extending into the duct lumen. The periductal stromal is often cellular and oedematous.
Benign, no risk of malignancy.

69
Q

RFs for atherosclerosis

A

Age
Sex
Genetics
Hyperlipidaemia
Hypertension
Smoking
Diabetes Mellitus

multiplicative risk factors

70
Q

Characteristics of stable vs unstable plaque

A
71
Q

Manifestations of IHD

A

Angina pectoris
Myocardial infarction
Chronic IHD with heart failure
Sudden cardiac death.

72
Q

% stenosis for unstable angina

A

90%

73
Q

Leading cause of sudden cardiac death

A

coronary artery disease

74
Q

Virchow’s triad

A

blood
vessel wall
blood flow

75
Q

low sodium high potassium diagnosis

A

addisons

76
Q

Urgent treatment for phaeo

A

alpha blocker (e.g. phenoxybenzamine)

then you can add a beta blocker and arrange surgery

77
Q

types of adrenal tumours causing high BP

A

pheochromocytoma (catecholamine secreting tumour)
conn’s syndrome (aldosterone secreting tumour)
Cushing’s syndrome (cortisol secreting tumour)

78
Q

Surgery for adrenal tumours

A

remove the entire adrenal (more straightforward and less bleeding then when trying to resect a piece)

79
Q

signs of hypovolaemia

A

tachycardia
reduced urine output
postural hypotension
dry mucous membranes
confusion / drowsiness
reduced skin turgor

!!!!!!!low urine sodium (<20)!!!!!! -> if you are deficient in sodium, you will not excrete that much.

80
Q

treatment for hypovolaemic hyponatraemia

A

volume replacement with 0.9% saline

81
Q

how do you treat a euvolaemic patient with hypo Na+?

A

fluid restriction
treat underlying cause

82
Q

What is the % of hypertonic saline?

A

3% NaCl

83
Q

when would you give 3% (hypertonic saline)

A
  • reduced GCS
  • seizures
  • seek senior/expert help
84
Q

How do you treat hyperNa+?

A

fluid replacement
treat the underlying cause

85
Q

What is more common, HL or NHL?

A

Non-Hodgkin’s Lymphomas 80%
Hodgkin Lymphoma 20%

86
Q

What lymphoma is associated with EBV?

A

Burkitts

87
Q

histopathology starry sky appearance indicates

A

Burkitt’s lymmphoma

88
Q

Chemotherapy regimen for Hodgkin’s lymphoma

A

ABVD

2-6 cycles

curative

89
Q

Do you use radiotherapy in Hodgkin’s lymphoma?

A

often used alongside chemo in bulky areas or limited disease

however: very high risk of breast cancer in women

90
Q

Causes for appropriate raised EPO

A

High altitude
Hypoxic lung disease
Cyanotic heart disease
High affinity haemoglobin

91
Q

causes for inappropriate raised EPO

A

Renal disease (cysts, tumours inflammation)
uterine myoma
other tumours (liver, lung)

92
Q

clinical presentation of essential thrombocytosis

A

Incidental finding on FBC (50% cases)
Thrombosis: arterial or venous
CVA, gangrene, TIA
DVT or PE
Bleeding: mucous membrane and cutaneous
Headaches, dizziness visual disturbances
Splenomegaly (modest)

93
Q

Management of essential thrombocytosis

A

Aspirin: to prevent thrombosis
Hydroxycarbamide: antimetabolite. Suppression of other cells as well.
Anagrelide: specific inhibition of platelet formation, side effects include palpitations and flushing

94
Q

aetiology of CNS tummours

A
  • largely unknown
  • previous head and neck radiation
  • family history
95
Q

What cancers most commonly give rise to brain mets?

A

breast
melanoma
renal
lung

96
Q

prognosis of CNS mets

A

very poor

97
Q

What is the most common brain tumour in children?

A

pilocytic astrocytoma

98
Q

what does CNS tumour grade tell us?

A

survival

g1: benign, long term survival
g2: >5y
g3: <5y
g3: <1y

99
Q

What is the most common CNS tumour in adults?

A

metastatic

100
Q

normal ICP for supine adult

A

7-15 mmHg

101
Q

epidemiology of stroke

A

3rd most common cause of death in the UK

leading cause of disability

102
Q

what is the most common cause of non-traumatic intra parechnymal bleed?

A

hypertension

103
Q

Main causes of subarachnoid haemorhages

A
  • berry aneurysm
  • htn
104
Q

what % poeple have berry aneurysms?

A

1%

105
Q

Risk factors for CNS infarctoin

A

cerebral ATHEROSCLEROSIS

smoking
diabetes
htn

106
Q

haemorrhage behind ear sign name

A

battle sign

classic of a skull base fracture

107
Q

chronic traumatic encephalopathy

A

patients presenting with psychiatric signs

environmentally triggered degenerative process

108
Q

Define metaplasia

A

changing of one type of epithelium into another; it is reversible;

109
Q

Barret’s oesophagus

A
  • columnar lined eosophagus (rather than squamous)
  • with goblet cells: intestinal metaplasia
  • without goblet cells: gastric metaplasia
  • reversible
110
Q

What is the main cause of duodenal ulcers?

A

H. pylori

111
Q

Whipple’s disease

A

caused by trypherma whippelii

can cause duodenal ?ulcers/?itis

112
Q

Histological features of coeliac disease

A

villous atrophy

lymphocytes in tissue

113
Q

what are opportunistic infections?

A

An infection caused by an organism that does not normally cause disease

114
Q

serology

A

Measure levels of antibody in patients serum

115
Q

CMV treatment (with SE)

A

Ganciclovir (IV): bone marrow suppression
Valganciclovir: oral
Foscarnet (IV) (nephrotoxicity)
Cidofovir (nephrotoxicity)
IVIg (with another drug for pneumonitis)

116
Q

what are the different risks of CMV in patients posts SOT and HSCT

A
116
Q

What are the main cells in the liver?

A

hepatocytes
bile ducts (epithelial cells)
blood vessels
endothelial cells
kupffer cells -> when activated become myofibriblasts
stellate cells (store vitamin a)

117
Q

components of the hepatic triad

A
118
Q

complications of liver cirrhosis s

A

portal htn
hepatic encephalopathy
cancer

119
Q

What is spotty necrosis of the live indicative of?

A

acute hepatitis

(could be caused by viruses Orr drugs)

120
Q

Potts fracture

A

ankle fracture
includes fibula and tibia

121
Q

Band keratopathy

A

calcium in the eye

due to hypercalcaemia

if you see this it is unlikely to be cancer

122
Q

osteitis fibrosis and cystic

A

can occur in long standing hyperparathyroidism

rare

loss of bone mass

123
Q

RFs for calcium errand stones

A

FH
dehydration
hypercalciuria (>6mmol Ca/day)
hypercaalcaemia
HPTH

124
Q

Ix for renal calcium stones

A

KUB
stone analysis
urine and serum biochemistry

125
Q

Mx of renal calcium stones

A

lithotripsy
cystoscopy
lithotomy

drink lots and let the stones pass

126
Q

How to manage primary hyperparathyroidism?

A

Acute: rehydration! fluids, fluids, fluids; 4L saline/day if they don’t have heart failure. If the calcium falls a tiny bit, you are winning.

Don’t give bisphosphonates.

avoid thiazides
Later: surgery

Year 5 😊✌🏼 (53 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions