Brainscape's Knowledge GenomeTM

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


See full index

Year 2 - Endocrinology (DP) > Pathology > Flashcards

Pathology Flashcards

1
Q

What is the basic pathophysiology of T2DM?

A
  1. Insulin receptors become less sensitive to insulin
  2. Less glucose enters cells
  3. Hyperglycaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What causes insulin resistance?

A

Ectopic fat accumulation
Increased FFA circulation
Increased CRP
Reduced glycogen synthesis

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

How does insulin resistance affect β-cells?

A

Results in:
- Hyperglycaemia
- Lipotoxicity (Increased FFA + triglycerides)
These reduce β-cell function

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

What kind of obesity is associated with increased risk of T2DM and CVS disease?

A

Central

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

What is central obesity associated with?

A

Metabolic syndrome:

 - High BP
 - High triglycerides
 - Low HDL
 - Insulin resistance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the thyroid gland mainly composed of?

A

Follicles:
- Surrounded by flat/cuboidal epithelial cells
- Thyroglobulin in centre (amorphic and pink)
Scattered C cells:
- Parafollicular

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

What do C cells look like?

A

Slightly larger than follicular cells

Clearer cytoplasm

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

What function do C cells have?

A

Secrete calcitonin:

- Reduces serum calcium

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

What does TSH do?

A
  1. Binds to TSH-receptor on epithelial cells
  2. G-proteins activated:
    • GTP -> GDP
    • Production of cAMP
      > Increased production/release of T3 + T4
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What two forms do T3 and T4 circulate in?

A

Bound

Free

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

When T3 and T4 bind to target cell receptors, what happens?

A
  1. Complex translocates to nucelus
  2. Binds to thyroud response elements on target genes
  3. Transcription increases
  4. Increased basal metabolic rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the most common cause of hyperthyroidism?

A

Grave’s disease

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

What is the male:female ratio for Grave’s disease?

A

10:1

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the peak age range for Grave’s disease?

A

20-40

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

What autoantibodies are present in Grave’s disease?

A

TSH receptor
Thyroid peroxisomes
Thyroglobulin

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

What autoantibody is relatively specific in Grave’s?

A

Anti-TSH receptor (Thyroid stimulating)

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

What autoantibody may explain hypothyroid episodes?

A

TSH binding inhibitor Ig

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

What is the triad of features in Grave’s disease?

A

Hyperthyroidism with diffuse thyroid enlargement
Exophthalmos:
- Fibroblasts express TSH receptors
Pretibial myxoedema

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

What is the most common cause of hypothyroidism?

A

Hashimoto’s Thyroiditis (Autoimmune)

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

What are some associations for Hashimoto’s?

A

Middle aged women
Other autoimmune disease
HLA-DR3 + HLA-DR5

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

What age do people get Hashimoto’s Thyroiditis?

A

45-60 years old

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What has been shown in twin studies for Hashimoto’s?

A

Autoantibodies are present in asymptomatic siblings

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

What do polymorphisms in CTLA-4 cause?

A

Dysregulation of T cell responses
Reduced protein level and function:
- Increased risk of autoimmune disease

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

What does PTPN-22 normaly do?

A

Inhibits T cell function

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

What autoantibodies are present in Hashimoto’s Thyroiditis and what happens when they’re bound?

A

Anti-Thyroglobulin and Anti-Peroxidase
When bound:
- Ab-dependent cell mediated cytotoxicity

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

What cells may mediate thyroid epithelium destruction?

A

CD8 positive cells

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

What is the process of cytokine mediated cell death?

A

IFNγ:

- Recruits macrophages -> Damages follicles

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

What is Hashitoxicosis?

A

When Hashimoto’s Thyroiditis is preceded by transient hyperfunction

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

What does Hashimoto’s predispose to?

A

Other autoimmune disease

B-cell non-Hodgkin’s Lymphoma in affected gland

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

What is a goitre?

A

Any thyroid enlargement

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

In what populations is there an increased incidence of diffuse goitre?

A

Females
Pubescent
Young adults

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

How else can diffuse goitre arise?

A

Ingesting substances which reduce T3/T4 production
Dyshormonogenesis:
- Cretinism (in kids)
Mostly idiopathic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How does diffuse goitre usually present?

A

Euthyroid:
- T3/T4 normal
- TSH raised
Mass effects

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

How does a Multi-Nodular Goitre arise?

A

Long-standing simple goitre:

 - Recurrent hyperplasia + involution
 - Impressive enlargement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is a differential of multi-nodular goitre?

A

Neoplasm

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

What is the pathogenesis of multi-nodular goitre?

A

Follicle rupture -> Haemorrhage -> Scarring -> Calcification

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

What mass effects can multi-nodular goitre have?

A

Cosmetic
Airway obstruction
Dysphagia
Vessel compression

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

How does an autonomous multi-nodular goitre present?

A

Hyperthyroid

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

What is the most common cause of a goitre?

A

Iodine deficiency:

 - Lack of intake
 - Lack of bioavailability
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What type of neoplasm appears a discrete solitary mass encapsulated by a surrounding collagen cuff?

A

Thyroid adenoma

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

What is a thyroid adenoma difficult to distinguish from?

A

Dominant nodule in MNG

Follicular carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

If a thyroid adenoma secretes thyroid hormones, is it classed as TSH-dependent or TSH-independent?

A

TSH-independent

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

What mutations can cause a thyroid adenoma?

A

RAS

PIK3CA

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

What mutations are seen in functional thyroid adenomas?

A

TSHR signalling pathway:

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

What people are at greatest risk of thyroid carcinomas?

A

Females

Early adulthood

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

Ionising radiation predisposes to what type of thyroid cancer?

A

Papillary

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

Iodine deficiency predisposes to what type of thyroid cancer?

A

Follicular

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

What genetic features are seen in papillary cancer?

A

Active MAP kinase pathway:

 - Rearrange RET/NTKR1
 - BRAF point mutation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

What genetic features are seen in follicular cancer?

A

Mutations in PI3K/AKT

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

What genetic features are seen in anaplastic cancer?

A

MAP kinase mutations
PI3K/AKT mutations
p53 + -catenin mutations

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

What genetic features are seen in medullary cancer?

A

MEN2 (Germline RET mutations)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is the structure of a papillary thyroid carcinoma?

A

Solitary nodule:

 - Can be multifocal
 - Often cystic
 - May be calcified
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What worsens the prognosis of a papillary thyroid cancer?

A

Age >40
Extra-thyroid extension
Distant metastases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is the structure of a follicular thyroid carcinoma?

A 
Usually a single nodule:
     - Enlarges slowly
     - Painless
     - Non-functional
May surround capsule
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Where do medullary thyroid carcinomas arise from?

A

C cells:

 - Neuroendocrine
 - Can secrete calcitonin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

What can medullary thyroid carcinomas be related to?

A

MEN2A or MEN2B:

- Often presenting in younger patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

How do familial medullary thyroid cancers appear?

A

Bilateral/Multicentric

C cell hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

What are medullary thyroid carcinomas composed of?

A 
Spindle/Polygonal cells
Arranged in:
     - Nests
     - Trabeculae
     - Follicles
59
Q

What deposits are seen in medullary thyroid cancer?

A

Amyloid (abnormally folded calcitonin)

60
Q

What effects do medullary thyroid cancers have?

A 
Mass:
     - Dysphagia
     - Hoarseness
     - Airway obstruction
Paraneoplastic:
     - Diarrhoea (VIP production)
     - Cushing's (ACTH production)
61
Q

What is the most undifferentiated and aggressive thyroid carcinoma?

A

Anaplastic

62
Q

What are the parathyroid glands composed of? What do they look like and what do they secrete?

A 
Chief cells:
     - Round
     - Moderate cytoplasma
     - Bland, round, central nuclei
Secrete PTH
63
Q

What are the supporting cells in the parathyroid gland? What do they look like?

A

Oxyphil cells:

 - Larger
 - Acidophilic cytoplasm
64
Q

What is parathyroid hyperplasia associated with?

A

MEN1 and MEN2A

65
Q

How does a parathyroid adenoma appear?

A 
Single gland -> 0.5-5grams
Other glands are atrophic
Microscopically represents normal glands
Fibrous CT capsule:
     - Adjacent rim of compressed tissue
66
Q

What happens in secondary hyperthyroidism?

A

Chronic hypocalcaemia:

- Results in compensatory overactivity

67
Q

What are signs of secondary hyperthyroidism?

A

Renal failure
Low calcium intake
Vitamin D deficiency

68
Q

What happens in tertiary hyperparathyroidism?

A

Autonomous activity

Associated with hypercalcaemia

69
Q

What are the signs of hyperparathyroidism?

A 
Bones
Stones (Kidney and Gallstones)
Groans (Constipation/Peptic ulcer/Pancreatitis)
Psychic overtones
CVS:
     - Aortic/Mitral calcification
70
Q

What specific bone problem can hyperparathyroidism cause?

A

Osteitis Fibrosa Cystica

71
Q

What can DiGeorge syndrome cause? What is the mutation seen?

A

Congenital absence of thyroid and parathyroid glands:
- Hypoparathyroidism
Chromosome 22q11.2

72
Q

What is familial hypoparathyroidism associated with?

A

Primary adrenal insufficiency (Addison’s)

Mucocutaneous candidiasis

73
Q

What are signs of hypoparathyroidism?

A 
Tetany:
     - Neuromuscular irritability
     - Chvostek's and Trousseau's Signs
Basal ganglia calcification
Parkinsonian
Increased ICP:
     - Papilloedema
Cataracts
QT prolongation
74
Q

What is the adenohypophysis and where is it derived from?

A

Anterior pituitary

Derived from Rathke’s Pouch

75
Q

What is the neurohypophysis and where is it derived from?

A

Posterior pituitary
Extension of neural tissue:
- Modified glial cells
- Axonal processes

76
Q

What hormones are secreted by the anterior pituitary?

A 
Trophic:
     -TSH, ACTH, FSH, LH
Non-trophic:
     - GH
     - PRL
77
Q

What hormones are secreted by the posterior pituitary?

A

ADH

Oxytocin

78
Q

How is the anterior pituitary composed histologically?

A 
Acidophils:
     - Somatotrophs -> GH (50%)
     - Mammotrophs -> PRL (20%)
Basophils:
     - Corticotrophs -> ACTH (20%)
     - Thyrotrophs -> TSH (5%)
     - Gonadotrophs -> FSH/LH (5%)
Chromophobe
79
Q

Are the axons forming the posterior pituitary myelinated or not?

A

No

80
Q

What can cause anterior pituitary hyperfunction?

A

Adenoma

Carcinoma

81
Q

What can cause anterior pituitary hypofunction?

A 
Surgery/Radiation
Haemorrhage (Apoplexy)
Ischaemic necrosis (Sheehan Syndrome)
Tumours extending into sella
Sarcoidosis
82
Q

What conditions affect the posterior pituitary?

A 
Diabetes insipidus:
     - Lack of ADH secretion
SIADH:
     - Ectopic secretion (tumour)
     - Primary pituitary disorder
83
Q

What percentage of intra-cranial tumours are pituitary adenomas?

A

10%

84
Q

What disorder is pituitary adenoma associated with? What is this condition called?

A

MEN1 -> Wermer Syndrome

85
Q

What size is a microadenoma and what size is a macroadenoma?

A

Micro is 1cm

86
Q

How do we classify pituitary adenomas?

A

By cell type/hormone produced

87
Q

Are all pituitary adenomas functional?

A

No:

- 25-30% are hypofunctional/non-functional

88
Q

True or false; if a pituitary adenoma is functional, hormones can be secreted at a subclinical level?

A

True

89
Q

What subset of pituitary adenomas are aggressive?

A

Those with p53 mutations and many mitotic figures

90
Q

What can large pituitary adenomas cause?

A

Bitemporal hemianopia
Pressure atrophy
Infarct -> Panhypopituitarism

91
Q

What does a PRL-secreting pituitary adenoma cause?

A

Infertility
Decreased libido
Amenorrhoea

92
Q

What does a GH-secreting pituitary adenoma cause?

A 
GH -> Increased IGF
Stimulates growth of:
     - Bone
     - Cartilage
     - Connective tissue
Gigantism/Acromegaly
93
Q

What does a ACTH-secreting pituitary adenoma cause?

A

Cushing’s
Usually Micro
BAH

94
Q

True or false; Pituitary hypofunction is usually panhypopituitarism?

A

True

95
Q

What tumours can cause pituitary hypofunction?

A

Rathke Cleft cysts

96
Q

What causes of granulomas can cause pituitary hypofunction?

A

Sarcoidosis

TB meningitis

97
Q

How does a patient with apoplexy present?

A 
Headache
Diplopia (CN iii pressure)
Hypopituitarism
CV collapse
Loss of consciousness
98
Q

What hypothalamic tumours can cause pituitary hypofunction?

A 
Benign:
     - Craniopharyngioma
Malignant:
     - Glioma
     - Metastases
99
Q

Where are craniopharyngiomas derived from?

A

Rathke’s pouch

100
Q

What are the features of craniopharyngiomas?

A

Slow growing
Often cystic
May calcify

101
Q

Where do most craniopharyngiomas arise?

A

Suprasella

102
Q

What ages are craniopharyngiomas most common?

A

Bimodal:

 - 5-15 years
 - 50-60 years
103
Q

How do craniopharyngiomas present?

A

Headache
Visual disturbance
Reduced growth in children

104
Q

What is central diabetes insipidus and what can cause it?

A 
ADH deficiency
Caused by:
     - Trauma
     - Tumours
     - Inflammation
105
Q

What is nephrogenic diabetes insipidus?

A

Renal resistance to ADH

106
Q

Where re the adrenal glands located?

A

Superomedial to the upper pole of the kidneys

107
Q

What are the three zones of the adrenal cortex (from superficial to deep)? What are the functions of each?

A

Zona glomerulosa:
- Produces mineralocorticoids + aldosterone
Zona fasciculata:
- Produces glucocorticoids + cortisol
Zona reticularis:
- Produces sex steroids + glucocorticoids

108
Q

What nerves innervate the adrenal medulla?

A

Pre-synaptic SNS fibres

109
Q

What cells are in the adrenal medulla and what do they secrete?

A 
Neuroendocrine/Chromaffin cells:
     - Secrete catecholamines
               > Adrenaline
               > NA
               > Small amount of dopamine
110
Q

What other diseases can manifest in the adrenal gland?

A

Pituitary -> ACTH secretion
Shock/DIC
Conditions damaging gland

111
Q

What three general pathologies can cause adrenal hyperfunction?

A

Hyperplasia
Adenoma
Carcinoma

112
Q

What can cause acute and chronic adrenal hypofunction?

A 
Acute:
     - Waterhouse-Friderischsen
               > Haemorrhage after Neisseria meningitidis
Chronic:
     - Addison's
113
Q

What mode of inheritance is CAH?

A

Autosomal recessive

114
Q

What is the pathogenesis of CAH?

A

1) 21-hydroxylase deficiency
2) Reduced steroid synthesis:
- No cortisol or aldosterone production
3) Increased androgen production -> Virilisation

115
Q

What does the decreased cortisol in CAH result in?

A

ACTH release

Cortical hyperplasia

116
Q

What can cause acquired adrenal hyperplasia?

A

Endogenous ACTH:
- Pituitary adenoma -> Cushing’s Disease
- Ectopic ACTH -> Small Cell LC
Bilateral adrenal enlargement

117
Q

What are the types of adrenal enlargement?

A

Diffuse -> ACTH driven

Nodular -> ACTH-independent

118
Q

What should you suspect if there is an adrenocortical tumour in children?

A

Li-Fraumeni syndrome

119
Q

What can an adrenocortical carcinoma present with?

A

Fever (due to necrosis)

120
Q

A well-circumscribed and encapsulated adrenocortico tumour. Approximately 2cm diameter, with a yellow-brown cut surface.

A

Adrenocortical adenoma

121
Q

How can an adrenocortical carcinoma spread?

A 
Locally:
     - Retroperitneum
     - Kidney
Vascular spread to liver, lungs and bone
Peritoneum and pleura
Regional LNs
122
Q

What features suggest an adrenocortical carcinoma?

A 
Large size:
     - >50g
     - >20cm
Haemorrhage + necrosis
Frequent and atypical mitoses
Capsular/Vascular invasion
123
Q

What can adrenocortical adenomas resemble and how?

A

Cortical cells:

 - Well differentiated
 - Small nuceli
 - Rare mitotic figures
124
Q

What can cause a massive adrenal haemorrhage?

A

Newborn
Anticoagulants
Disseminated Intravascular COagulation (DIC)
Waterhouse-Friderichsen

125
Q

What are the three common causes of chronic adrenal insufficiency?

A 
Autoimmune destruction
Infection:
     - TB
     - Fungal (Histoplasma)
     - HIV
Metastases (Lung and breast)
126
Q

How much of the adrenal gland needs to be destroyed for there to be symptoms?

A

> 90%

127
Q

What biochemical results are seen in Addison’s?

A 
Hypoglycaemia
Hyperkalaemia
Hyponatraemia
Hypovolaemia
Hypotension
128
Q

What can cause an Addisonian crisis?

A

Infection

Surgery/Trauma

129
Q

Where do adrenal medullar neuroblastomas arise?

A

40% from medulla

60% along sympathetic chain

130
Q

What is the general composition of a medullar neuroblastoma?

A

Primitive cells

May show maturation to ganglion cells

131
Q

What features worsen the prognosis of a adrenal medulla neuroblastoma?

A

N-myc amplification

Telomerase expression

132
Q

What cells is a phaeochromocytoma derived from?

A

Chromaffin cells in the adrenal medulla

133
Q

What can a phaeochromocytoma cause?

A

Paroxysmal secondary hypertension:

 - Stress/Exercise/Posture/Tumour palpation
 - Micturition
134
Q

Which of the following is not a complication of phaeochromocytomas:

  • CHF
  • MI
  • CVA
  • PAD
  • Arrhythmia
A

PAD

135
Q

How is phaeochromocytoma diagnosed biochemically?

A

Urinary:

 - Catecholamines
 - Metabolites
136
Q

Phaeochromocytomas are the 10% tumour. What does this mean?

A 
10% are extra-adrenal:
     - Paragangliomas
     - Organs of Zuckerkandl
     - Carotid body
10% are bilateral
10% are malignant
10% are NOT associated with hypertension
137
Q

What percentage of Phaeochromocytomas are familial? What are features of familial Phaeochromocytomas?

A

25%:

 - Germline mutations
 - Younger and bilateral
 - 30% malignant if β-subunit of succinate dehydrogenase mutation
138
Q

What features of a phaeochromocytoma suggest it is malignant?

A

Large

Necrotic

139
Q

How do phaeochromocytomas appear?

A

Yellow and red-brown
BUT can vary up to
Haemorrhagic and necrotic

140
Q

What makes phaeochromocytomas appear brown?

A

K2Cr2O7:

- Oxidises catecholamines

141
Q

What do tumour cells in a phaeochromocytoma form?

A

Nests (Zellballen)

142
Q

What syndrome are phaeochromocytomas a feature of?

A

MEN2A -> Sipple Syndrome

and also MEN2B

143
Q

What causes MEN2A and what are they at risk of?

A 
RET oncogene germline mutations -> 10q11.2
They have:
     - Phaeochromocytomas
     - Medullary thyroid cancer
     - PTH hyperplasia
144
Q

What causes MEN2B and what are they at risk of?

A 
RET point mutations
They have:
     - Phaeochromocytomas
     - Medullar thyroid cancer
     - Neuromas
     - Ganglioneuromas
     - Marfanoid habitus

Year 2 - Endocrinology (DP) (15 decks)

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