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Endocrine System > Pathology > Flashcards

Pathology Flashcards

1
Q

What are the causes of Hypopituitarism ?

A
  • Tumours ( Primary/Metastatic)
  • Pituitary apoplexy - bleeding into pituitary tumour
    *Ischaemic necrosis ( Sheehan’s syndrome
    *Trauma
  • Iatrogenic- radiation for cerebral tumours
  • Inflammation - Bacterial/Viral meningitis, chronic sinusitis, osteomylitis
  • Genetic abnormalities
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2
Q

What is the most common cause of Hyperpituitarism?

A

Pituitary Adenoma

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3
Q

What is the most frequent type of functioning Pituitary adenoma?

A

Lactotroph adenoma

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4
Q

What are the clinical features of a Lactotroph adenoma?

A

In Females - Amenorrhoea, Infertility , Galactorrhea

Males- Gynaecomastia, Galactorrhea

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5
Q

What is the treatment for a Lactrotroph Adenoma?

A

Bromocriptine /Surgical removal

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6
Q

What are types of Adrenocortical hyper- function?

A
  • Increase in cortisol - Cushing’s syndrome
  • Increase in aldosterone - Hyperaldosteronism
  • Increase in Androgens - Adrenogenital / virilizing syndromes
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7
Q

What are the types of Adrenocortical hypo function?

A
  • Primary acute adrenocortical insufficiency - Adrenal crises
  • Primary Chronic adrenocortical insufficiency ( Addison’s disease)
  • Congenital adrenal hyperplasia
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8
Q

What are the different types of Hyperaldosteronism?

A

Primary (most common) & Secondary

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9
Q

What are causes of Primary Hyperaldosteronism ?

A
  • Bilateral idiopathic hyperaldosteronism- characterized by bilateral nodular hyperplasia of the adrenal glands.
  • Adrenocortical neoplasm (aldosterone- producing adenoma)
  • Overactivity of the aldosterone synthase gene, CYP11B2.
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10
Q

What is Conn’s syndrome?

A

This is a solitary aldosterone-secreting adenoma in the zona glomerulosa of the adrenal gland cortex.

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11
Q

What is the cause of Secondary Hyperaldosteronism ?

A

In secondary hyperaldosteronism, aldosterone release occurs in response to activation of the renin-angiotensin system.

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12
Q

What is the most important feature of Hyperaldosteronism ?

A

Hypertension

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13
Q

What is the most common cause to secondary hypertension?

A

Primary hyperaldosteronism

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14
Q

What is the major histological feature of an aldosterone- secreting adenoma?

A

Spironolactone bodies

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15
Q

What is the best treatment for patients with Primary Hyperaldosteronism due to bilateral hyperplasia?

A

Aldosterone antagonist such as spironolactone.

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16
Q

An adrenocortical adenoma is often symptomatic with no hormone production but when it does produces hormones, which ones are being produced?

A

Cortisol & Aldosterone

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17
Q

In which condition is an Adrenocortical adenoma mostly seen?

A

Multiple Endocrine Neoplasia Syndrome (MEN -1)

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18
Q

What are the rare causes of Adrenal carcinoma?

A

Li-Fraumeni syndrome and Beckwith-Wiedemann syndrome

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19
Q

What happens to the Renin levels in Primary Hyperaldosteronism?

A

It is LOW

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20
Q

In what conditions are Secondary Hyperaldosteronism seen?

A
  • Decreased renal perfusion (arteriolar nephrosclerosis, renal artery stenosis)
  • Arterial hypovolemia and edema (congestive heart failure, cirrhosis, nephrotic syndrome)
  • Pregnancy (caused by estrogen-induced increases in plasma renin substrate.
  • Juxtaglomerular cell tumors (renin-producing)
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21
Q

What happens to the Renin levels in Secondary Hyperaldosteronism?

A

It is HIGH

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22
Q

What are the causes of Adrenal Insufficiency ( Hypofunction of Adrenal gland)?

A
  • Primary adrenal disease (primary hypo- adrenalism)
  • Decreased stimulation of the adrenals resulting from ACTH deficiency (secondary hypoadre- nalism)
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23
Q

Fill in the blanks. “ Primary adrenocortical insufficiency may be ______ or _______.”

A

Acute (called adrenal crisis), or Chronic (Addison disease).

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24
Q

What are the causes of Acute adrenal insufficiency?

A

(1)Sstopping prescribed corticosteroids without a tapering period, or
(2) Bilateral adrenal hemorrhage (Waterhouse-Friderichsen syndrome)

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25
Q

What are the clinical findings associated with Bilateral adrenal hemorrhage (Waterhouse-Friderichsen syndrome)?

A
  • Bilateral adrenal hemorrhage can occur during sepsis, especially with Neisseria meningitides meningococcemia.
  • The endotoxin that is secretes can lead to disseminated intravascular coagulation (DIC) and adrenal hemorrhage, called Waterhouse- Friderichsen syndrome.
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26
Q

What are the causes of Addison’s disease?

A
  • Autoimmune adrenalitis
  • Miliary tuberculosis
  • AIDS
  • Metastatic cancer
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27
Q

What are the clinical features associated with Addison’s disease?

A

(1) Hyponatremia with a hyperkalemic metabolic acidosis caused by loss of aldosterone.

(2) Hypoglycemia caused by loss of cortisol.

(3) Hypotension caused by loss of both aldosterone and cortisol.

(4)Hyperpigmentation

(5) Eosinophilia

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28
Q

In which type of Diabetes is the Beta cells of the pancreas destroyed and thus eliminating production of insulin?

A

Type I Diabetes Mellitus

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29
Q

Describe Type II diabetes mellitus?

A

This occurs when there is insulin resistance combined with inability of Beta cells to produce appropriate amounts of insulin.

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30
Q

Which type of Diabetes mellitus is more common?

A

Type II

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31
Q

Fill in the blanks. “ Type I DM is characterized by an absolute deficiency of insulin caused by _________.”

A

An autoimmune attack on the Beta cells of the pancreas.

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32
Q

Type I diabetes are normally found in what type of persons?

A

Persons during childhood or puberty

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33
Q

What is the triad seen in patients with Diabetes mellitus?

A
  • Polyuria (frequent urination)
  • Polydipsia (excessive thirst)
  • Polyphagia (excessive hunger)
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34
Q

Which test is normally used to identify Gestational diabetes in pregnant women?

A

The oral glucose tolerance test.

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35
Q

True or False? When blood glucose is greater than 180 mg/dl, the ability of the kidneys to reclaim glucose is impaired. This results in glucose “spilling” into the urine. The loss of glucose is accompanied by the loss of water, resulting in the characteristic polyuria (with dehydration) and polydipsia of diabetes

A

TRUE!!

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36
Q

What are the Hallmarks of untreated Type I diabetes ?

A

Elevated levels of blood glucose and ketone bodies.

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37
Q

Which enzyme is the substrate for ketogenesis in Diabetic ketoacidosis?

A

Acetyl Coenzyme A

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38
Q

What hormones are secreted in response to Hypoglycemia?

A

Glucagon and epinephrine

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39
Q

What genes are associated with Type I diabetes mellitus?

A
  • HLA-DR3 and HLA-DR4 in whites.
  • HLA-DR7 in African Americans
  • HLA-DR9 in Japanese people
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40
Q

True or False? Insulin resistance increases with weight gain.

A

TRUE!!

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41
Q

What is the pathophysiology of burnshock?

A
  • CARDIAC – cytokines affecting contractility and loss of volume.
  • Renal- hypovolemia and raised harmatocrit with myoglobin
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42
Q

Fill in the blanks. “ Tissue damage in burns is due to the transfer of _______.”

A

Energy

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43
Q

What are the types of energy that can be transferred in a burn injury?

A

Thermal
Chemical
Electrical
Radiation

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44
Q

What are the different types of Burn?

A
  • Flame
  • Scald
  • Chemical
  • Electrical
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45
Q

Which type of Burn is a Full thickness burn?

A

Third Degree burn

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46
Q

What type of Burn is a partial thickness burn and can be superficial or deep?

A

Second degree burn

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47
Q

What is the healing time for a first degree burn?

A

5 days

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48
Q

What are the clinical features of a First degree burn?

A
  • Affects epidermis only
  • Erythema
  • Minimal oedema
  • Painful
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49
Q

Second degree burns ( Partial thickness burn) affects what layer of the skin?

A

All of the epidermis and parts of the dermis

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50
Q

What are the clinical features of a Second degree burn?

A

Blistering
Reddish /whitish
Painful

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51
Q

What is the healing time for a second degree burn?

A

10-28 days

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52
Q

Third degree burns ( Full thickness burns) affects what layer of the skin?

A

All the epidermis and dermis

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53
Q

True or False? Full thickness burns have a healing time of one year.

A

FALSE!! They cannot heal due to destruction of all skin elements.

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54
Q

What are the clinical features of a Third degree burn( Full thickness)?

A

White
Leathery
Pain FREE

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55
Q

What are the “ soft signs” for a respiratory tract injury due to burns ?

A
  • Closed space fires ( guess this is the type of fire idk tbh)
  • Facial burns
  • Singing of facial hair
  • Oropharygeal carbon deposits
  • Carbonaceous sputum
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56
Q

What are the “ hard signs” for a respiratory tract injury due to burns?

A
  • Dyspnea
  • Chest tightness
  • Tachypnea
  • Stridor
  • Oedema of tongue or oropharynx
  • Full Thickness burns to face
  • Circumferential neck burns
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57
Q

What is the treatment for a respiratory tract injury due to burns?

A
  • Early Intubations
  • Cricothyriodotmy
  • Tracheostomy
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58
Q

What are the diagnostic imaging used to determine a respiratory tract injury due to burns?

A
  • Bronchoscopy
  • Xenon Lung Scans
  • CT Scans
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59
Q

What are the major complications of a respiratory tract injury due to burns?

A

*Pulmonary oedema

*ARDS ( Acute respiratory distress syndrome)

*Pulmonary Embolism

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60
Q

How does Carbon monoxide poisoning affect cell function?

A

When it preferentially binds with the hemoglobin. It impairs mitochondrial function.

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61
Q

What is the normal values of CO?

A

0-5 PPM

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62
Q

A Carbon monoxide level of 20-40 Ppm will give what symptoms?

A

Disorientation, Fatigue, Nausea

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63
Q

What level of Carbon Monoxide will cause Combativeness and a coma?

A

40-60

64
Q

Carbon monoxide level of 15-20 will cause?

A

Headache, Confusion

65
Q

Carbon monoxide level of greater than 60 will cause?

A

Death

66
Q

What is the Treatment for patients with suspected Carbon Monoxide poisoning?

A

100% O2 (half life reduced from 4hrs to 45min)
- Hyperbaric Oxygen (HBO) Therapy

67
Q

Fill in the blanks. “Early Mortality in Burn patients was due to______.”

A

Acute renal failure

68
Q

What are the rule of nine’s?

A

These are used to determine area percentage of burns on the patient.

  • Head & neck - 9% (anterior & posterior)
  • Chest area - 36% ( anterior & posterior)
  • Right arm - 9%
  • Left arm- 9%
  • Right Leg- 18%
  • Left leg 18%
    Perineum - 1%
69
Q

What is the purpose of Parkland’s formula?

A

This is a calculation used to determine how much fluids should be given to a patient for the first 24 hours following a burn. The total amount of fluid needed is given in during 8 hour periods.

70
Q

What is the calculation for Parkland’s formula?

A

4ml X weight in kg X TBSA ( Total body surface area involved in the burn.

71
Q

What are escharotomies?

A

An escharotomy is an emergency surgical procedure involving incising through areas of burnt skin to release the eschar ( dead tissue that forms over healthy skin and then, over time, falls off (sheds) and its constrictive effects, restore distal circulation, and allow adequate ventilation.

72
Q

True or False? Escharotomies should be performed in a surgical operating theatre with the use of anaesthesia.

A

FALSE!!
* No need for anesthesia.
* Can be done at bedside.

73
Q

What are the different features to be looked at in Invasive monitoring of a burn patient?

A
  • 30% TBSA
  • CARDIAC DYSFUNCTION
    *PULMONARY DYSFUNCTION
  • RENAL DYSFUNCTION
74
Q

Doing a second survey of burn injuries what aspects should be looked at?

A
  • EYES NEED TO BE ASSESSED FOR CORNEAL DAMAGE.
  • ASSOCIATED INJURIES
75
Q

What is the criteria for Admission for Burn injuries?

A
  • Second-degree burns greater than 10%
  • TBSA in patients younger than 10 years or older than 50 years.
  • Second-degree burns greater than 20% TBSA in persons of other age groups.
  • Burns that involve the face, hands, feet, genitalia, perineum, or major joints.
  • Third-degree burns
  • Inhalational injury
  • Electrical burns, including lightening injury.
  • Chemical burns
  • Burn injury in patients with preexisting medical disorders.
  • Multiple Trauma.
  • Special Circumstances (Abuse).
  • Electrical burns, including lightening injury.
  • Chemical burns
  • Burn injury in patients with preexisting medical disorders.
  • Multiple Trauma
  • Special Circumstances (Abuse)
76
Q

What are the Phyisical sensory (pain) management for Burn injuries?

A

Narcotics
- Intravenous
- Titrated

77
Q

What are the Phyisiological sensory management for Burn injuries?

A

Distraction therapy ex music , art

78
Q

What is the micro-organism (infection) management for burn injuries?

A
  • Tetanus treatment
  • Bacterial treatment
  • Topical antimicrobial
  • Fungal
  • Prologed partenteral antibiotics
  • High mortality
79
Q

What are examples of Topical microbial used in the treatment for burn injuries?

A
  • Silver nitrate
  • Silver sulfadiazine
  • Mafenide acetate
  • Povidone (“Betadine”)
  • Topical Gentamycin
80
Q

True or False? Silver Nitrate can cause eschar penetration while Silver sulfadiazine has CANNOT penetration eschar.

A

FALSE !! Silver Sulfadiazine CAN penetrate eschar while silver nitrate CANNOT penetrate eschar.

‘SS can penetrate’

81
Q

Which other topical microbial can cause penetrate Eschar?

A

Mafenide acetate

82
Q

True or False? Silver sulfadiazine is painful.

A

FALSE!! It is painless

’ SS is painleSS’

83
Q

What is the main adverse effect of silver nitrate?

A

Causes electrolyte imbalances & discolouration

84
Q

What is the main adverse effect of silver sulfadiazine?

A

Causes neutropenia transiently

85
Q

What is the main adverse effect of Mafenide acetate ?

A

Metabolic acidosis leads to hyper ventilation

86
Q

What enzyme is inhibited by the drug Mafenide acetate ?

A

Carbonic hydrase

87
Q

True or False? Silver agents should NOT be applied to the head and neck areas due to hyperpigmentation.

A

TRUE!!

88
Q

What are the goals of dressings of a Burn injury ?

A

Protect the damaged epithelium
Reduce evaporative losses
Reduce pain
Reduce infections

89
Q

True or False? Open wound dressings can cause an increase in infection while closed wound dressings can increase evaporation and heat losses.

A

FALSE!!

  • Open wounds increase evaporation and heat loss
  • Close wounds increase infection if NOT changed properly.
90
Q

Fill in the blanks. “ Open wound dressing _______the wound while Closed wound dressing can _______ the wound.”

A

Open wound dressing - can Observe the wound

Closed wound dressing - Debrides the wound

90
Q

True or False? Closed wounds dressings are more expensive than open wounds dressing .

A

TRUE!! Duhhh

91
Q

What type of knife is used in a Tangenital burn excision ( Skin graft knives)?

A

Humby or Silvers knife
- via the papillary or reticular dermis

92
Q

What are examples of Temporary skin substitutes?

A
  • Porcine Grafts
  • Cadaveric Grafts
  • Amniotic Membrane
93
Q

What are examples of Skin graft knives?

A

Humby knife
Silvers knife
Dermatome knife
Mesher knife
Carriers knife

94
Q

What is the treatment of burn wound sepsis?

A
  • Surgical Excision
  • Systemic Antibiotics
  • Emperic
  • Culture Directed- Tissue and Blood
95
Q

What are the effects of burn injuries on the gastrointestinal tract?

A
  • Nasogastric compression
  • Stress ulceration prophylaxis ( curling ulcers)
  • Nutrition
96
Q

What is the difference between the Harris Benedict Formula and the Curreri Formula?

A

The Curreri formula (25 kcal/kg + 40kcal/TBSA burn) overestimates caloric needs of the burn patient (as estimated by calorimetry) by 25% to 50%. The Harris-Benedict formula underestimates the caloric needs of the burn patient (as estimated by calorimetry) by 25% to 50%.

97
Q

The Iceberg concept is associated with which type of burns?

A

Electrical burns

98
Q

What are the effects of Electrical burns?

A
  • Cardiac Injury
  • Arrhythmias
  • Renal Injury
  • Myoglobinuria
99
Q

True or False? Hypertrophic scars limit to area of injury and regress while keloids extend beyond the area of injury.

A

TRUE!!

100
Q

True or False? Flaps have No blood supply while Grafts have a blood supply.

A

FALSE!! Flaps have a Blood supply while Grafts DO NOT have blood supply.

101
Q

Autografts are from ?

A

The same individual

102
Q

Xenografts are from ?

A

From animals

103
Q

What type of treatment is essential for Keloids?

A
  • Adjuvant therapy is a must.
  • Superficial radiotherapy.
  • Triamcinolone acetate.
  • Pressure therapy.
104
Q

What are the clinical features of Acromegaly?

A
  • Elongation of long bones
  • Protruding jaw (prognathism)
  • Thickening of phalanges
  • Over growth of visceral organs
  • Widening of the teeth
  • The hands and feet are enlarged
  • The fingers are broad and sausage-like
105
Q

Which type pf Pituitary adenomas produces a local mass effect?

A

Non-functional pituitary adenoma.

106
Q

What is the most common type of genetic abnormalities associated with pituitary adenomas ?

A

G-protein mutations

107
Q

Which genes are associated with causing familial pituitary adenomas?

A

MEN1, CDKN1B, PRKAR1A, and AIP

108
Q

What is the most frequent type of Hyperfunctioning Pituitary adenoma?

A

Lactotroph adenoma

109
Q

Fill in the blanks. “ If a growth hormone– secreting adenoma develops BEFORE THE EPIPHYSES close, as is the case in prepubertal children, excessive levels of growth hormone and ( Insulin-like growth factor 1) IGF1 result in ________.”

A

Gigantism

110
Q

What is the role of IGF1?

A

Persistent growth hormone excess stimulates the hepatic secretion of insulin-like growth factor 1 (IGF1), which acts in conjunction with growth hormone to induce overgrowth of bones and muscle.

111
Q

What stain gives a positive Corticotoph adenoma?

A

Periodic acid–Schiff (PAS) ) - stains, as a result of the accumulation of glycosylated ACTH protein.

112
Q

Fill in the blanks. “ Patients with Nelson syndrome present with _________.”

A

Patients present with the mass effects of the pituitary tumor

113
Q

What are the local mass effects of Pituitary neoplasms?

A
  • Radiographic abnormalities of the sella turcica, including sellar expansion, bony (crinoid process) erosion, and disruption of the diaphragma sellae.
  • Bitemporal hemianopsia
  • Elevated intracranial pressure
  • Headaches, nausea, and vomiting
  • Seizures ( or obstructive hydrocephalus)
  • Cranial nerve palsy.
  • Pituitary apoplexy ( acute hemorrhage into a pituitary neoplasm is associated with rapid enlargement of the lesion and loss of consciousness)
  • Thrombosis of ICA
114
Q

What type of adenoma is a Corticotroph adenoma?

A

A basophil adenoma

115
Q

True or False? Chromphobe adenomas are Hyperfunctioning.

A

FALSE!! They are non-functioning

116
Q

A lack of ADH results in ?

A

Diabetes Insipidus

117
Q

What are the causes of anterior pituitary hypofunction ?

A
  • Tumors and other mass lesions (especially nonfunctioning pituitary adenomas)
  • Ischemic necrosis of the anterior pituitary, called Sheehan syndrome.
  • Iatrogenic causes - include ablation of the pituitary by surgery or radiation.
  • Sarcoidosis or tuberculosis, trauma,
  • Primary or metastatic tumors involving the pituitary.
  • Pituitary apoplexy
118
Q

A deficiency in growth hormone will result in?

A

Pituitary dwarfism

119
Q

What are the causes of The syndrome of inappropriate ADH (SIADH) - excess ADH?

A
  • The secretion of ectopic ADH by malignant neoplasms (particularly small-cell carcinomas of the lung)
  • Non- neoplastic diseases of the lung,
  • Local injury to the hypothalamus or neurohypophysis.
120
Q

What are the effects of Parathyroid Hormone?

A
  • Increased renal tubular reabsorption of calcium
  • Increased urinary phosphate excretion, thereby lower- ing serum phosphate levels (since phosphate binds to
    ionized calcium)
  • Increased conversion of vitamin D to its active dihy-
    droxy form in the kidneys, which in turn augments
    gastrointestinal calcium absorption
  • Enhanced osteoclastic activity (i.e., bone resorption,
    thus releasing ionized calcium), mediated indirectly by promoting the differentiation of osteoclast progenitor cells into mature osteoclasts
121
Q

What are the two genetic associations of parathyroid tumours?

A
  • Cyclin D1 gene rearrangements
  • MEN1 mutations
122
Q

What is used to determine the diagnosis for Parathyroid Hyperplasia?

A

Inraoperatuve Frozen section

123
Q

What are the common causes of Hypoparathyroisim?

A
  • Surgical removal of parathyroids during thyroidectomy.
  • Congenital absence: This occurs in conjunction with thymic aplasia (Di George syndrome) and cardiac defects.

*Autoimmune hypoparathyroidism: This is a hereditary polyglandular deficiency syndrome arising from auto- antibodies to multiple endocrine organs ( mutation in the autoimmune regulator (AIRE) gene)

124
Q

True or False? During Intraoperative frozen section of the Parathyroid gland, if there is Hypercellular parathyroid gland then there is Examination of ONE gland?

A

TRUE!!

125
Q

True or False? During Intraoperative frozen section of the Parathyroid gland, If there is If normal / atrophic —–> Adenoma If hypercellular / enlarged → Hyperplasia then you should examine another parathyroid gland.

A

TRUE!!

126
Q

What is the diagnostic criteria for Diabetes?

A
  1. A fasting plasma glucose greater than or equal to 126 mg/dL, and/or
  2. A random plasma glucose greater than or equal to 200 mg/dL (in a patient with classic hyperglycemic signs, discussed later), and/or
  3. A 2-hour plasma glucose greater than or equal to 200 mg/dL during an oral glucose tolerance test with a loading dose of 75 gm, and/or
  4. A glycated hemoglobin (HbA1C) level greater than or equal to 6.5% (glycated hemoglobin is further discussed under chronic complications of diabetes)
127
Q

What are the Causes of Secondary diabetes?

A

(A) Exocrine pancreatic ts
 Pancreatectomy
 Chronic pancreatitis
 Haemachromatosis
 Neoplasia

(B) Endocrinopathies
 Cushings syndrome  Glucagonoma

(C) Drugs
 Corticosteroids (glucocorticoids)
 Thyroid hormone
 Thiazides
 Phenytoin (dilantin)
 Interferon-α
 Protease inhibitors (HIV)

(D) Infections
 CMV, Cocksackie virus B

128
Q

What is the main function of insulin?

A

↑ rate of glucose transport into cells eg. skeletal muscle
→ ↑ source of energy

129
Q

Fill in the blanks.” Chronic complications of Diabetes results in MACROvascular diseases which causes _______.”

A

Accelerated atherosclerosis among diabetics, resulting in increased myocardial infarction, stroke, and lower extremity ischemia.

130
Q

Fill in the blanks.” Chronic complications of Diabetes results in MICROvascular diseases which affects ares such as _______.”

A

Retina, kidneys, and peripheral nerves, resulting in diabetic retinopathy, nephropathy, and neuropathy, respectively

131
Q

What are the pathogenesis in the Chronic complications of Diabetes?

A

1.Formation of advanced glycation end products (AGEs).
2. Activation of protein kinase C
3.Disturbances in polyol pathways.

132
Q

How are Advanced Glycosylation End Products (AGEs) formed?

A

They are formed by binding of glucose derived molecules to amino groups of protein.

133
Q

What is the name of the receptor to which AGE’s bind to which is expressed on inflammatory cells (macrophages and T cells), endothelium and vascular smooth muscle?

A

RAGE receptor

134
Q

What happens when AGE binds to the RAGE receptor?

A
  • Release of cytokines and growth factors, including transforming growth factor β (TGFβ), which leads to deposition of excess basement membrane, and vascular endothelial growth factor (VEGF), implicated in diabetic retinopathy.
  • Generation of reactive oxygen species (ROS) in endothelial cells
  • Increased procoagulant activity on endothelial cells and macrophages.
  • Enhanced proliferation of vascular smooth muscle cells and synthesis of extracellular matrix
135
Q

What is the other mechanism through which AGE’s can produce its effects?

A

AGEs can directly cross-link extracellular matrix proteins. These cross- linked proteins can TRAP other plasma or interstitial proteins; for example, low-density lipoprotein (LDL) or albumin accelerating atherosclerosis and diabetic retinopathy .

136
Q

How does the activation of Protein Kinase C cause chronic complications in diabetics?

A
  • PKC activation are numerous and include production of PRO- ANGIGENIC molecules such as vascular endothelial growth factor (VEGF), implicated in the neovascularization seen in diabetic retinopathy.
  • Profibrogenic molecules such as transforming growth factor β, leading to increased deposition of extracellular matrix and basement membrane material.
137
Q

How does Disturbances in polyol pathway lead to chronic complications of Diabetes?

A

Tissues that does’t require insulin for glucose transport ex kidneys, nerves, blood vessels leads to an increase in intracellular glucose. This increase in glucose causes is then metabolized by the enzyme aldose reductase to sorbitol, a polyol, and eventually to fructose, in a reaction that uses NADPH . NADPH is required in a reaction that helps to regenerate glutathione (GSH). Low GSH leads to oxidative stress

  • The sorbitol caused also causes cellular swelling an direct toxicity .
138
Q

What are examples of the tissues that are DO NOT require insulin for glucose transport?

A

 Lens
 Nerves
 Kidney
 Blood vessels

139
Q

Fill in the blanks.” Chronic complications of diabetes can cause ________ which is as a result of advanced vascular disease?

A

Gangrene of the lower extremities

140
Q

What are the lesions seen in Diabetic nephropathy?

A

(1) Glomerular lesions
(2) Renal vascular lesions, principally arteriolosclerosis
(3) Pyelonephritis, including necrotizing papillitis (papillary necrosis) - pattern of acute pyelonephritis.

141
Q

What are the most important glomerular lesions?

A
  • Capillary basement membrane thickening
  • Diffuse mesangial sclerosis
  • Nodular glomerulosclerosis (Kimmelstiel-Wilson lesion) - Found in 15% to 30% of individuals with long-term diabetes and is a major contributor to renal dysfunction.
142
Q

What are the Ocular complications of diabetes?

A

Glaucoma
Cataracts
Diabetic retinopathy

143
Q

What is the most common Ocular complication of diabetes?

A

Diabetic retinopathy

144
Q

What are the two types of retinopathy?

A

Non- proliferative retinopathy and proliferative retinopathy.

145
Q

What is Non- proliferative retinopathy?

A

Includes intraretinal or preretinal hemorrhages, retinal exudates, microaneurysms, venous dilations, edema, and, most importantly, thickening of the retinal capillaries (microangiopathy).

  • Retinal exudates can be “soft” (microinfarcts) or “hard” (deposits of plasma proteins and lipids)
146
Q

What is Proliferative retinopathy?

A

Thiss a process of neovascularization and fibrosis. This lesion leads to serious consequences, including blindness, especially if it involves the macula

147
Q

What is the earliest manifestation of Diabetic nephropathy?

A

The appearance of small amounts of albumin in the urine (>30 but <300 mg/ day).

148
Q

Fill in the blanks. “ Diabetic neuropathy occurs as a result of Sorbiatal accumulation which leads to damage of _________ which can cause Peripheral neuropathy.”

A

Schwann cells

149
Q

What are the major causes or morbidity in Diabetes?

A

End stage renal disease
Loss of vision
Lower limb amputations

150
Q

Major causes of death from chronic complications of diabetes are?

A

Myocardial Infarction
Renal failure
Bacterial infections

151
Q

Which Glomerular lesions occurs because of hyaline material beneath epithelium of Bowman’s capsule?

A

Capsular drop

152
Q

Which Glomerular lesions occurs because of hyaline material beneath podocytes of Glomerulus?

A

Fibrin cap

153
Q

What is Insulin resistance?

A

Insulin resistance is defined as the failure of target tissues to respond normally to insulin.

154
Q
A

Endocrine System (10 decks)

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