Brainscape's Knowledge GenomeTM

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


See full index

pathology > Intro to pathology & disease causes > Flashcards

Intro to pathology & disease causes Flashcards

1
Q

Health

A

complete physical, mental and social well being

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

disease

A

malfunctioning of body or mind

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

Etiology

A

Whats the cause

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

Pathology

A

structural & functional abnormalities that are expressed as diseases of organs/systems

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

pathogenesis

A

how the etiologic agents cause a disease i.e morphological & functional chnge

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

lesion

A

unit of abnormality -anatomical

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

symptoms

A

what a patient complains abt e.g pain , restlessness, anxiety

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

signs

A

what doctors detects on exam. e.g lump, irregular heart beat

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

inflammation

A

red, swell, hot, pain, loss of function

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

prognosis

A

prospect of recovery or survival from disease

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

epidemiology

A

study of causes, distro & control of disease in a pop

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

syndrome

A

disease chrcterised by multi. abnormalities e.g downs syndrome (mental &heart defects)

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

lesion

A

structuraal abnorm. results from sickness e.g rash, growth on skin, patch of dead heart muscle in myocardial infarction

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

4 types of etiological agents

A

evnt , genetic, immuno, metabolic disorders

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

envt etiological agents

A

physical, chem, nutritional, infections, radiation, psychological

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

genetic factors

A

genes , sex

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

immunological causes

A

sle, rhEUMATOID ARTHIRITS

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

diseases from multifactorial etiological agents

A

diabetes ; hypertension; cancer

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

causative agent

A

infectious (bacterial, fungal,viral, parasitic, genetic, nutritional (kwashiorkor)

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

inflammatory / degenerative/ neoplastic are ex. of _________- of diseases

A

classification

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

how long is acute classification & chronic classification of disease

A

a - days-w / chronic = m/yrs

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

Do the systems inv. act as a class of disease

A

yes i.e cardiov; resp. ; NS, endocrine IS etc

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

Whats the difference bw primary & 2ndary causes of disease

A

primary has unknown cause & 2nd has known cause

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

Whats the name of abnormality present at birth

A

congenital

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

Are congenital abnorms always genetic

A

no cos some can develop during pregnancy and not in mum or dad = acq.

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

2 classes of tumours

A

benign/ malignant

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

How can the characteristics of disease be explained using…

A

Etiology / pathogenesis (mechanism) / manifestations (morph., functional & clinic chnge (signs & symptoms) / complications (2nd effects) prognosis = outcome & diagnosis (signs &symps = lab invest)

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

4 components to describe pathogenesis of a disease

A

aetiology , pathogenesis . signs & symptoms & complications

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

Describe pathogenesis of skin abscess (pus fat eye)

A

etiology = staph. aerus infects soft tissue ; patthogenesis = acute inflamm. & NpH from bld invade to destroy norm tissue ; in doing it - NpH killed liberating lysosomal enzymes which kill norm tissue at infection site
signs & symptoms = pus from dead tissue & dead NpH aka skin abscess
complications = septicemia if infection enters BVs

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

aetiology = etiology

A

yes

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

Describe pathogenesis of lung cancer

A

etio - cig smoke (has carcinogens that mutate cells)
p - mutation in genetic material
s&s - mutate = cancer in organs i.e lung tumour
comp - metastasis - when canc.cells spread via blood or lymphatic vessels & make 2ndary tumours in other organs

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

cirrhosis of liver

A

etio - Hep.B virus infects liver via blood
p- IR to HB kills infected LIVER cells & virus
s&s = liver cell death severe infection = - dead cells replaced by fibrous hard (scar) tissue = hardening of liver aka cirrhosis = liver failure
comp= both cirrhosis & liver failure

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

Hypertension Pathogenesis

A

etio - high bp from smoke ; clogged arteries ; high salt ; obesity etc.
p- varies ex: increased renin prod. for kidneys
s&s; none until heart,arteries & other organs damaged - dmge artery facilitates clot form = blood block to organ ; high bp etc.
comp = stroke / heart attacks; haemorrhage

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

Whats the prognosis for lung cancer patient (sqaumous cell Ca)

A

SURVIVAL 5 yrs , 15-20%

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

Prognosis of small cell lung ca

A

5 yr survival, 5%

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

myocardial infarction prognosis

A

survival: 10 yrs, 50%

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

3 terms to report a disease

A

prevalence incidence and mortality rate

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

diff bw prevalence & incidence rate

A

prevalence = total no. of patients (old & new) in given time but incidence is total no. of new cases only in a time period

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

mortality rate

A

no of total deaths/ total no. of people in pop per unit of time typically expressed as no. of deaths typically per 1000 individs per year

40
Q

how to calc incidence rate

A

total new cases in time period divided by size of pop at risk

41
Q

calc for prevalence rate

A

total no. of old & new patients in pop divided by no. of individs in pop at given timee

42
Q

3 most common diseases in developing (low income) countries

A

lower resp. infections ; HIV/AIDS ; diarrhoeal

43
Q

common disease in high income countries

A

ischaemic heart disease ; stroke ; trachea,bronchus lung infection

44
Q

What is kwashiorkor

A

protein-energy malnutrition characterised by oedema & enlarged liver w fatty infiltrates

45
Q

Gauchers disease

A

rare genetic disorder - lipids typically accum. in liver/spleen

46
Q

Whats the TORCH complex in congenital diseases

A

non-genetic causes of congenital disease ; Toxoplasma Others Rubella Virus Cytomegalovirus & Herpres simplex virus

47
Q

Cytogenetics

A

study of analysis of number & strctre of human & animal chromosomes

48
Q

What period in gestation is the dvpmt of major organs

A

weeks 5-8 ; embryo susceptible to effects of teratogens @ this time

49
Q

What infection does rubella cause & what are its secondary effects (defects from it)

A

intrauterine inf; causes cardiac, cerebral, opthalmic & auditory defects in fetus

50
Q

What are the similar abnormalities within the TORCH complex

A

brain, eyes, liver & grwth retardationprod. by fatal or neonatal infection

51
Q

Name some problems a baby exposed to alcohol in the womb can have

A

poor grwth (in wmb & after b) small head or jaw ; thin upper lip ; smooth pilthum (ridge bw nose & lip) ; cerebral palsy ; learning disorders; behavioural problems

52
Q

What is latrogenic syndrome

A

fetal alcohol syndrome

53
Q

What is thaidomide in latrogenic

A

immunomod. drug used as trmt of cancers i.e myeloma & comp. of leprosy - causes birth defects in babies if used on preggers

54
Q

Describe is toxoplamosis pathogenesis , route & symptoms

A

from inf. w toxoplasma gondii parasite ; route via eating undercook. contam. meat ; infected cat faeces exposure or mum-kid transmission in preggers.
symtpms of inf. newborn = seizures, enlarged liver, spleen & eye infection

55
Q

NAME chrosomal abnormalities that can cause disease

A

deletion; inversion ; translocation

56
Q

Whats ch. translocation

A

abnrom from rearranged parts bw nonhomologous ch.s ; detected on cytogenetics or karyotype of affected cells

57
Q

what does it mean to have unbalanced or balanced chromosome translocation

A

b - even xchnge of material w no gen. info extra,m missing yet functioning
unb - xhnge of chromosome material unequal = extra or missing genes

58
Q

disease examples from unbalanced ch. translocation

A

male infertility ; duchenne muscular dystrophy ; burkitts lymphoma ; papillary thyroid cancer

59
Q

Whats a ch.inversion & when does it occur

A

rearrangement where segment of a ch is reversed end to end ; occurs when single ch. breaks & rearranges within itslef ; simple rearrangement of linear ch. sequence

60
Q

What ch. undergoes inversion commonly seen in humans

A

ch.9

61
Q

Is ch. translocation harmful or any loss of genetic info

A

no

62
Q

Whats a deletion

A

mutation where ch. or DNA seq. is lost during DNA rep. ; any no. of nts can be deleted

63
Q

What can cause deletions

A

errors in ch.crossover during meiosis = several serious genetic diseases

64
Q

do deletions that dont occur in multiples of 3 bases cause frameshift by chnging the 3 nt protein reading frame of sequence

A

yes

65
Q

Example of disorders from medium sized deletions

A

Williams syndrome

66
Q

What ch. rearrangement can cause Cri du chat syndrome & what is CDC

A

deletion; characterised by mewing cat cry, mental retard and devpmt defect

67
Q

What is 5q- syndrome and its cause

A

caused by deletion ; defective dvpmt of RBCs = RBC shortage

68
Q

3 types of diseases from gene mutations

A

inherited defective genes : mono/polygenic ; mitochondrial inheritance & acq. defective genes

69
Q

Whats the difference between the two types of inherited defective genes

A

monogenic - single cell i.e CF, sicklec anaemia ; polygenic - multi i.e diabetes, bronchiol asthma

70
Q

How are genes mitochondrially inherited

A

mito genes inherit. by maternal transmssn ; have db circular DNA ; 100% chance each kid can inherit a mito.disease i.e mitochondrial myopathy

71
Q

whats mtDNA

A

mitochondrial DNA ; 50-100 mito per cell ; mtDNA codes for 13 pps in O2Phosph. .. needed for key systems so mutations to mito can be very impactful on humans

72
Q

Give 2 examples of mutation induced diseases

A

sickle cell anemia & cancer

73
Q

describe THE MUTATION responsible for sickle cell anaemia

A

SINGLE AA CHNGE in beta globin (codon for aa 6) of haemoglobin = SCA ; single nt sub (A to T mutation) chnges glutamic acid codon to valine codon = HbS (haemogobin form in SCA ppl)

74
Q

what codon change causes SCAnaemia & on what no. chrosome is the B-globin (HBB) gene on

A

glutamic acid GAG to valine GTG ; gene located on chrosome 11/ 11p15.5;; comp of 3 exons & 147 aa protein

75
Q

Describe SCA disorder in genetic terms

A

auto recessive; full disease needs homozygous genotype (x2 HbS) ; 1 = heterozygous SCtrait (AS genot)

76
Q

What is sickle cell trait and how does it affect individs

A

heterozygous one copy of HbS gene ; phenotypically dominant trait ; individs normal but RBCs can sickle under low 02 pressure e.g high altitudes - AS individs exhibit phenotypic dom but still recessive genotypically

77
Q

Autosomal dominant

A

only one abnorm copy of paired gene is needed for disease manifest.

78
Q

Give 4 examples of ADominant diseases

A

neurofibromatosis ; polycystic kidney disease ; familial hypercholestremia; marfan syndrome

79
Q

outline neurofibromatosis

A

defective gene on ch.17 = multi nerve sheath tumour

80
Q

outline polycystic kidney disease

A

mutations in PKD-1 on ch.16

81
Q

Marfan syndrome

A

fibrillin 1 gene mutation on ch.15 - disorder of CTissue, long limbs and defect in heart/aorta

82
Q

familial hypercholestrolemia

A

characterized by high cholesterol levels, specifically very high levels of low-density lipoprotein (LDL, “bad cholesterol”), in the blood and early cardiovascular disease. About 1 in 300 to 500 people have mutations in the LDLR gene that encodes the LDL receptor protein, which normally removes LDL from the circulation, or apolipoprotein B (ApoB), which is the part of LDL that binds with the receptor; mutations in other genes are

83
Q

familial hypercholestrolemia

A

characterized by high cholesterol levels, specifically very high levels of low-density lipoprotein (LDL, “bad cholesterol”), in the blood and early cardiovascular disease. About 1 in 300 to 500 people have mutations in the LDLR gene that encodes the LDL receptor protein, which normally removes LDL from the circulation, or apolipoprotein B (ApoB), which is the part of LDL that binds with the receptor; mutations in other genes are

84
Q

3 examples of AR disease

A

inborn errors of metabolism: Tay-Sachs, pompe disease & gauchers ;;; beta- thalassemia & cyctsicF

85
Q

CF

A

presence of mutations in both copies of the gene for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. Those with a single working copy are carriers and otherwise mostly normal. CFTR is involved in production of sweat, digestive fluids, and mucus. When CFTR is not functional, secretions which are usually thin instead become thick. The condition is diagnosed by a sweat test and genetic testing.
CFTR functions as an ATP-gated anion channel, increasing the conductance for certain anions (e.g. Cl−) to flow down their electrochemical gradient. The CFTR is found in the epithelial cells of many organs including the lung, liver, pancreas, digestive tract, reproductive tract, and skin. Normally, the protein moves chloride and thiocyanate ions (with a negative charge) out of an epithelial cell to the covering mucus. Positively charged sodium ions follow passively, increasing the total electrolyte concentration in the mucus, resulting in the movement of water out of the cell via osmosis. Defective CFTR results in reduced transport of sodium chloride and sodium thiocyanate in the reabsorptive duct and therefore saltier sweat. This was the basis of a clinically important sweat test for cystic fibrosis before genetic screening was available.

86
Q

X linked recessive diseases

A

rare in fems ; Haemophilia A (clotting fctr VIII deficiency- Xq28) rare bleeding disorder of abnorm clotting ; X-linked agammaglobulinemia ; duchenne musc.dystrophy

87
Q

Describe the 2 Diseases from abnormal sex chromosomal number

A

Turner - 45X (fem short , webbed neck, undvpd ovaries)
Klinefelters syndrome 47XXY (men w fem type pubic hair, small testicles, wide hips , breasts)

88
Q

Down syndrome

A

abnorm somatic ch.no ; common cause of intellectual disability (1/3) ; john down in 1866 described it and 1959 disc. presence of extra ch.21 is cause

89
Q

down syndrome trisomy 21

A

extra copy of ch.21 or atleast a segment of it ; intellect disability = IQ bw 25-70

90
Q

Describe downs syndrome

A

short body parts; flat nose; increased risk of leuk or. immuno deficiencies ; mental retard characterised by deposition of amyloid glycoprotein

91
Q

50% cases with congenital heart defects come from DS

A

true

92
Q

How Does incidence of DSyndrome change with increasing maternal age (MA)

A

Increases from MA 20 : 1 in 500 incidence @ birth to 1 in 30 at MA 40

93
Q

2 bacteria types that cause diseases

A

gram positive & negative

94
Q

endotoxin vs exotoxin

A
95
Q

endotoxin vs exotoxin

A

SLID ETABLES

96
Q

exotoxin

A

gram pos ; secreted by growing cells usually in protein form and neutralisation by antitoxin USE TABLE ON SLIDE

97
Q

VIRUSES

A

LAST SLIDE TO DO

pathology (6 decks)

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