Test 1 Flashcards

1
Q

• Define the metabolic disorders

A
OBESITY
•MALNUTRITION and DEFICIENCES
DISEASES
•CARBOHYDRATES- Diabetes
mellitus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

List the conditions associated with obesity

A
CONDITIONS ASSOCIATED WITH OBESITY
• Diabetes mellitus:
• Increased resistance to insulin.
• 80% of patients with NIDDM are
obese.
• Hypertension:
• Are 8x more likely to hypertensive.
• Atherosclerosis
• MI is more common.
• Gallstones and gallbladder
disease
Osteoarthritis.
• Complications following
surgery.
• Respiratory complications:
• Hypoventilation
syndrome.
• Cancer:
• Endometrium and breast.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

List the pathological findings in a patient with kwashiorkor

A
• There is protein deficiency
with:
• Muscle wasting
• Failure to grow
• Hypoproteinaemia mainly
hypoalbuminaemia
• Oedema
• Body fat is maintained.
Underweight but oedematous
due to hypoalbuminaemia (due
to adequate CHO but  protein
(essential amino acids)
• Depigmentated hair and skin
rash
• Secondary infections and
lethargy
• Fatty liver
Enzymes are low resulting in
multiple metabolic upsets.
• Anaemia due to inadequate
synthesis of haemoglobin.
• Decreased immune response
with thymic atrophy leading to
susceptibility to infections.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Discuss the pathogenesis of the signs of kwashiorkor i.e, oedema,
ascites, enlarged liver

A
• Skeletal muscles appear
wasted and pale.
• Heart: small and heart failure.
• Pancreas is atrophic.
• Intestines – villous atrophy.
• Liver – marked fatty change
• Infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

• List and discuss the complications of Vitamin A

A
Characterized by ocular
complications which may
cause permanent blindness:
• Night blindness d/t decreased
rhodopsin regeneration
• Xerophthalmia
• Keratomalasia
• Squamous metaplasia of
epithelium in other parts of
the body
• Bronchopneumonia
• Kidney stones
• Folicular hyperkeratosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

• Discuss the main presentation of Vitamin B complex

A
• Water soluble
• Thiamine or vit B1
• Generally widely available in
the diet
• Deficiency occurs in chronic
alcoholics and in some Asian
countries
• 3 main methods of
presentation:
• Polyneuropathy in a glove and
stocking distribution (dry beriberi)
• A high output cardiac failure
with oedema (wet beri-beri)
• Wernicke-Korsakoff syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

• List the clinical features of niacin b3

A
  • Causes pellagra
  • The clinical features incl:
  • Dematitis of the exposed parts
  • Diarrhoea
  • Dementia
  • Death if untreated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

• Compare and contrast type 1 and type 2 diabetes mellitus

A
Diabetes mellitus
IDDM (type 1)
• Less common
• Younger
• Thin
• Viral/autoimmune
• No insulin
• MHC class II link and
concordance 40%
• Ketotic coma
NIDDM (type 2)
• Increasingly common
• Older
• Obese
• Resistance to insulin
• Normal insulin
• No MHC link but
concordance 100%
• Hyperosmolar coma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

• Discuss the complications of diabetes mellitus

A
Accelerated atherosclerosis
and micro-angiopathy → MI,
stroke, PVD
• Renal – glomerulosclerosis →
chronic renal failure
• Retinopathy, cataract,
glaucoma
• Infections (renal, other, NB
fungi)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

The state of nutrition can be measured by:

A
Body weight.
• Subcutaneous fat as measured
by skinfold thickness.
• Muscle mass as measured by
mid-arm circumference.
• Serum proteins.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

RIBOFLAVINE DEFICIENCY

A
• Causes a sore tongue and
fissuring at the corners of the
mouth
• Dematitis
• Interstitial keratitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

DEFICIENCIES CAUSING ANAEMIA iron?

A
  • Iron deficiency

* Results in hypochromic microcytic anaemia.

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

DEFICIENCIES CAUSING ANAEMIA b12?

A
  • Vit B12
  • Is a water soluble vitamin.
  • Present in liver, milk, and eggs.
  • Is absorbed in the presence of IF secreted by the stomach
  • Necessary for nucleic acid and DNA formation
  • Deficiency results in megaloblastic anaemia.
  • Folic acid deficiency results in megaloblastic anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

b6 deficiency

A
VITAMIN B6
• May give rise to a type of
anaemia in which iron cannot
be used properly in the
formation of haemoglobin.
• Sideroblastic anaemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

VITAMIN D DEFICIENCY

A
• Rickets in children
• Results in excessive osteoid
production
• Deficient mineralisation
• Softening of bones, with
deformity and enlargement
• Osteomalacia in adults
• Softening and deformity of
bones d/t demineralsation
• There is low serum Ca2+ and a
high ALP
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

VITAMIN K DEFICIENCY

A
• A fat soluble vitamin
• Synthesized by gut bacteria
and absorbed in the presence
of bile
• Required for the formation of
prothrombin and factor V and
VII by the liver
• Deficiency leads to a
haemorrhagic state
17
Q

VITAMIN C DEFICIENCY

A
• Also known as scurvy
• One of the 1st deficiency
diseases to be discovered
• Essential for formation of
stable and strong collagen via
the hydroxylation of proline
• Complications stem from
weakness of collagen in blood
vessel walls
• Complications:
• Bleeding into the skin and from
the gums
• Subperiostial haematomas and
bleeding into joints
• Defective osteoid formation and
bony deformities in children
• Impaired wound healing
• Anaemia may follow bleeding
18
Q

Define inflammation

A
• It is a complex reaction of living tissue to an injury
• It is divided into two patterns:
Acute Inflammation 
Rapid onset
Short duration
lasts minutes to a few days
Oedema, predominantly neutrophils 

Chronic Inflammation:
Longer duration
Lymphocytes, macrophages, proliferation of blood
vessels and fibrosis

19
Q

Discuss the signs of acute inflammation

A

• The defining characteristic is the reaction of blood vessels. Resulting
in:
• Increased fluid (oedema) and leukocytesin the extravascular space.
• It is a protective mechanism.
• It destroys, dilutes and walls off harmful agents.
• It is closely intertwined with the process of healing and repair.
• It consists of:
1 A vascular response
2 Migration and activation of leukocytes
3 Systemic reaction

Signs of Inflammation heat, redness, swelling, pain ( loss of function by Virchow)

20
Q

• List the causes of acute and chronic inflammation

A
Exogenous(from outside the body) 
Trauma and physical injury
Infections
Including foreign material
Chemicals (acids, alkalis) 
Heat or Thermal Injury 
Radiation
Endogenous(from within the body)
Reaction to necrosis
Hypersensitivity reactions
Infarcts
Centre of tumours
 Immunological Reactions
Auto-immune diseases
Endogenous chemicals (e.g. Bile)
Metabolic products (e.g. Urate crystals)
21
Q

Discuss the three components of acute inflammation

A

Three components:
Vascular component
Changes in the caliber of vessels, resulting in increased blood flow
Exudative component
Structural changes in the microvasculature, resulting in increased permeability,
allowing plasma proteins and leukocytes to leave the microcirculation
Cellular component
The accumulation and activation of leukocytes at the site of injury

22
Q

Discuss the sequelae of acute inflammation

A
  • Resolution (usual result)
  • Suppuration
  • Pus formation (living and dead neutrophils, microorganisms, cellular debris)
  • An abscessis an accumulation of pus
  • Repair and organisation
  • Results in fibrosis
  • Chronic inflammation
23
Q

Describe the morphologic features of chronic inflammation

A
  • Infiltration by mononuclear inflammatory cells
  • Macrophages
  • Lymphocytes
  • Plasma cells
  • Tissue destruction
  • Induced by noxious stimulus or inflammation itself
  • Attempts at healing
  • Angiogenesis and fibrosis
24
Q

Discuss granulomatous inflammation

A

Granulomatous Inflammation
• specific pattern of chronic inflammation which results in an
accumulation of activate macrophages
• Granuloma: localised collection of modified macrophages (epitheliod
cells), may contain multinucleate giant cells
• Multinucleate giant cells are formed by fusion of epitheliod cells in
the presence of poorly soluble, indigestible material
• Granulomas may be surrounded by lymphocytes and, occasionally,
plasma cells

Epitheliod Cells
• Modified macrophages
• Large amount of pink,
pale cytoplasm (resemble epithelial cells)
• Possibly develop:
• In response to material that is
difficult to digest
• As a result of T cell-mediated delayed
hypersensitivity type of immune response
25
Q

• List the causes of granulomatous inflammation

A

Causes of Granulomatous Inflammation
• Bacteria:
• Tuberculosis (caseating granuloma)
• Tuberculoid leprosy (No central necrosis,
involvement of nerves)
• Yersinia enterocolitica (mesenteric lymphade
nitis
• Cat scratch disease
• Lymphogranuloma venereum
• Spirochaetes: tertiary syphilis: granulomatous inflammation around gummatous
necrosis
• Fungi e.g. Histoplasmosis, cryptococcosis
• Parasites e.g. Schistosomiasis
• Foreign material
• Inorganic: silica, talc, beryllium and zirconium
• Organic: starch, catgut sutures
• Insoluble material
• Keratin, elastic lamina, faecal material, sodium
biurate (gout), fat necrosis
• Cell mediated hypersensitivity
• TB, leprosy, rheumatiod nodules, inflammatory
bowel disease
• Unknown: sarcoidosis, Crohn’s disease

26
Q

Discuss the mechanism of healing

A

Granulation tissue is the red granular tissue that forms when a
wound heals
• Granulation tissue is composed of proliferating fibroblasts and new
blood vessels
• Formation of granulation tissue commences quite early on in
inflammation (when macrophages begin to accumulate)
• Formation of granulation tissue marks the beginning of chronic
inflammation

Angiogenesis;
⚫New blood vessels grow into the area from the surrounding normal
tissue and endothelial progenitor cells (EPCs) are recruited
⚫Angioblast-like cells are derived from the bone marrow
⚫The new vessels are more permeable initially than normal vessels,
allowing proteins to leak out. Thus, granulation tissue may be
oedematous.
⚫New vessels are stabilised by the recruitment of pericytes, SMCs and
ECM
⚫ Some of these vessels develop a muscular layer and become
arterioles, others dilate and become venules

Fibroblasts grow in from the surrounding normal tissue
• These produce proteoglycan ground substance initially. Later, they
lay down collagen fibres.
• Myofibroblasts form when fibroblasts form contractile proteins
• Lymphatic channels and nerves develop later.

27
Q

• List the factors influencing healing

A
• General
• Age, protein deficiency, Vit C deficiency, Zinc deficiency, Glucocorticoid
steroids
• Local
• Blood supply
• Infection
• Wound movement
• Amount of tissue destroyed
• Radiation
28
Q

• List the complications of healing

A
  • Infection of the wound
  • Overgrowth of the granulation tissue (“proud flesh”)
  • Contraction
  • Keliod formation
  • Pain (from neuroma or nerve fibres growing into the wound)
  • Weakness
  • Malignancy (e.g. chronic leg ulcer)