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Medicine: PBL wrap-ups > Unit 8 Week 2: Chlamydia and risky behaviour > Flashcards

Unit 8 Week 2: Chlamydia and risky behaviour Flashcards

1
Q

physiological functions of the liver

A

bile production
carbohydrate metabolism
lipid metabolism
protein and ammonia metabolism
storage functions

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2
Q

bile production liver

A

hepatocytes
into the bile canaliculi to smaller ducts then large ducts then eventually to the duodenum or gall bladder
following the secretion of bile into the duodenum undergoes enterohepatic circulation
bile components arent excreted are recylced by conversion into bile acids by gut bacteria for reuse by absorption in ileum

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3
Q

components of carbohydrate metabolism

A

glycogenolysis
gluconeogenesis
glycolysis
glycogenesis

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4
Q

glycogenolysis

A

liver can break down glycogen, stored form of glucose, into glucose-6-phosphate. This process is stimulated by the hormone glucagon

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5
Q

gluconeogenesis

A

liver can synthesis new glucose molecules from non carb resources such as amino acids, lactate, glycerol. This is stimulated by the hormones glucagon and cortisol

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6
Q

glycolysis

A

liver can also use glucose for energy, glucose is converted into pyruvate, enters citric acid cycle to generate ATP

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7
Q

glycogenesis

A

can store excess glucose as glycogen. Stimulated by the hormone insulin

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8
Q

componetns of lipid metabolism

A

lipogenesis
lipolysis
beta oxidation
lipoprotein metabolism

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9
Q

lipogenesis

A

process of synthesising new fatty acids from glucose, amino acids and other precursors. Synthesises and releases triglycerides, stored in adipose tissue as a long term energy source

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10
Q

lipolysis

A

breaking down and storing fat into fatty acids. Stimulated by hormones such as glucagon and adrenaline

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11
Q

beta oxidation

A

beta oxidation of fatty acids into acetyl-CoA, which then enters the citric acid to generate ATP

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12
Q

lipoprotein metabolism

A

involved in the synthesis and metabolism of lipoproteins which are responsible for transporting lipids through the body, low and high density lipoproteins

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13
Q

components of protein and ammonia metabolism

A

protein synthesis
amino acid catabolism urea cycle

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14
Q

protein synthesis

A

synthesis many plasma proteins, including albumin, fibrinogen and globulins, these proteins are responsible for maintaining osmotic pressure and transporting molecules

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15
Q

amino acid catabolism

A

breaks down amino acids, used for energy or synthesis or other molecules, converted to pyruvate, acetyl CoA or other intermediates that then enter the citric acid

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16
Q

urea cycle

A

converting toxic ammonia into urea, involves a series of enzymatic reactions that occur in the liver, resulting urea is excreted in the urine

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17
Q

storage functions of the liver

A

glycogen
vitamins
minerals
drug and toxin

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18
Q

glycogen storage

A

liver stores glycogen, broken down into glucose when the body needs energy

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19
Q

vitamin storage

A

storage of several vitamins, including vitamins A, D and b12, released into blood stream when needed

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20
Q

mineral storage

A

stores minerals such as Iron and copper, these are used for a variety of functions such as oxygen transport and enzyme function

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21
Q

drug and toxin storage

A

can store certain drugs and toxins, can accumulate in the liver overtime, can lead to liver damage or dysfunctions if it reaches toxic levels

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22
Q

pathophysiology of alcohol related liver disease

A

alcohol readily absorbed from stomach
mostly absorbed from the small intestine
cant be sotred
mainly catabolised in he liver by alcohol dehydrogenase, ADH and microsomal enzyme oxidation system, MEOS

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23
Q

alcohol metabolism via ADH pathways

A

ADH, a cytoplasmic enzyme, oxidizes alcohol into acetaldehyde.​

Acetaldehyde dehydrogenase (ALDH), a mitochondrial enzyme, then oxidizes acetaldehyde into acetate. ​

Chronic alcohol consumption enhances acetate formation.​

These oxidative reactions generate hydrogen, which converts nicotinamide-adenine dinucleotide (NAD) to its reduced form (NADH), increasing the redox potential (NADH/NAD) in the liver.​

The increased redox potential inhibits fatty acid oxidation and gluconeogenesis, promoting fat accumulation in the liver.

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24
Q

alcohol metaoblism via MEOS pathway

A

Chronic excessive alcohol consumption induces the MEOS (mainly in endoplasmic reticulum), increasing its activity. ​

The main enzyme involved is CYP2E1. ​

When induced, the MEOS pathway can account for 20% of alcohol metabolism. ​

This pathway generates harmful reactive oxygen species, increasing oxidative stress and formation of oxygen-free radicals.

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25
Q

hepatic fat accumulation

A

Fat (triglycerides) accumulates throughout the hepatocytes for the following reasons: ​

Export of fat from the liver is decreased because hepatic fatty acid oxidation and lipoprotein production decrease.​

Input of fat is increased because the decrease in hepatic fat export increases peripheral lipolysis and triglyceride synthesis, resulting in hyperlipidemia​

Hepatic fat accumulation may predispose to subsequent oxidative damage.

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26
Q

endotoxins in the gut due to alcohol

A

alcohol changes gut permeability
increases absorption of endotoxins released by bacteria in the gut
in response to the endotoxins which the impaired liver can no longer detoxify Kupffer cells release free radicals and increase oxidative damage

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27
Q

oxidative stress increases

A

Liver hypermetabolism, caused by alcohol consumption​

Free radical–induced lipid peroxidative damage​

Reduction in protective antioxidants (eg, glutathione, vitamins A and E), caused by- alcohol-related undernutrition​

Binding of alcohol oxidation products, such as acetaldehyde, to liver cell proteins, forming neoantigens and resulting in inflammation​

Accumulation of neutrophils and other white blood cells (WBCs), which are attracted by lipid peroxidative damage and neoantigens​

Inflammatory cytokines secreted by WBCs​

Accumulation of hepatic iron, if present, aggravates oxidative damage. Iron can accumulate in alcohol-related liver disease through ingestion of iron-containing fortified wines

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28
Q

resultant inflammation cell death and fibrosis as result of alcohol

A

A vicious circle of worsening inflammation occurs: ​

Cell necrosis and apoptosis result in hepatocyte loss, and subsequent attempts at regeneration result in fibrosis ​

Stellate (Ito) cells, which line blood channels (sinusoids) in the liver, proliferate and transform into myofibroblasts, producing an excess of type I collagen and extracellular matrix. ​

As a result, the sinusoids narrow, limiting blood flow. ​

Fibrosis narrows the terminal hepatic venules, compromising hepatic perfusion and thus contributing to portal hypertension​

Extensive fibrosis is associated with an attempt at regeneration, resulting in liver nodules. This process culminates in cirrhosis

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29
Q

cause of alcoholic fatty liver, steatosis

A

lipid accumulation:
FA uptake increases
lipogenesis increases
beta oxidation decreases
VLDL release decreases

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30
Q

cause of alcohol steatoheptatitis

A

inflammation:
kupffer cell activation
TLR4/NFKb pathway
cytokine/ ROS increases

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31
Q

cause of alcohol fibrosis/ cirrhosis

A

fibrosis:
protein adduct
PKC and TGF beta pathway
profibrotic effect of ROS

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32
Q

cause of heptatocellular carcinoma

A

carginogenesis:
DNA/protein adduct
dna integrity decreases
dna repair decreases

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33
Q

3 stages of alcohol related liver disease

A

alcoholic fatty liver disease
alcoholic heptatitis
cirrhosis

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34
Q

alcoholic fatty liver disease

A

Drinking a large amount of alcohol, even for just a few days, can lead to a build-up of fats in the liver. This is called alcoholic fatty liver disease, and is the first stage of ARLD.​

Fatty liver disease rarely causes any symptoms, but it’s an important warning sign that you’re drinking at a harmful level.​

Fatty liver disease is reversible. If you stop drinking alcohol for 2 weeks, your liver should return to normal.

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35
Q

alcoholic hepatitis

A

Alcoholic hepatitis – which is unrelated to infectious hepatitis – is a potentially serious condition that can be caused by alcohol misuse over a longer period. When this develops, it may be the first time a person is aware they’re damaging their liver through alcohol.​

Less commonly, alcoholic hepatitis can occur if you drink a large amount of alcohol in a short period of time (binge drinking).​

The liver damage associated with mild alcoholic hepatitis is usually reversible if you stop drinking permanently.​

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36
Q

liver cirrhosis

A

Cirrhosis is a stage of ARLD where the liver has become significantly scarred. Even at this stage, there may not be any obvious symptoms.​

It’s generally not reversible, but stopping drinking alcohol immediately can prevent further damage and significantly increase your life expectancy.​

A person who has alcohol-related cirrhosis and doesn’t stop drinking has a less than 50% chance of living for at least 5 more years.

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37
Q

treatment for alcohol related liver disease

A

no specific medical treatment
stop drinking
liver transplant may be required

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38
Q

effects of alcohol on gall bladder

A

Small amounts = reduce risk of gallstones and gallbladder pain ​

Heavy drinking = lead to gallbladder problems and pain

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39
Q

effects of alcohol on the brain physically

A

Difficulty walking​

Blurred vision​

Slurred speech​

Slowed reaction times​

Impaired memory​

Alcohol-related brain damage (ARBD), e.g Wernicke–Korsakoff syndrome

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40
Q

effect of alcohol on the brain psycholocially

A

depressant
affects inihibtion
depression
slows cognitive functioning

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41
Q

how cna dependency develop

A

long temr alcohol uses and reduces number of neurotransmitters in our brains
need some to ward off anxiety and depression so drink to relieve

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42
Q

alcohol damage to nerve cells

A

toxic
can cause brain cells to die
brain tissue shrink

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43
Q

damage to blood vessle alcohol

A

can lead to high blood pressure

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44
Q

alcohol and mental health

A

depression
anxiety
psychosis
suicide and self harm

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45
Q

chlamydia as a pathogen

A

Chlamydiae are gram-negative, obligate intracellular pathogens (require a eukaryotic host to replicate and for ATP).​

Chlamydia trachomatis and Chlamydia pneumoniae, the major species that infect humans.

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46
Q

pathophysiology of chlamydia

A

Elementary bodies bind to the host cell by the formation of a trimolecular bridges between bacterial adhesins, host receptors and host heparan sulfate proteoglycans (HSPGs).​

Pre-synthesised type III secretion system (T3SS) are needle-like molecular syringes, enable direct infection of bacteria effector molecules across host membranes. Some of these bacterial effectors initiate cytoskeleton rearrangement to facilitate endocytosis of the elementary body (known as inclusion). Elementary bodies can also be phagocytosed by leukocytes.​

Other bacteria effectors initiate mitogenic signalling to establish anti apoptosis state.​

Bacterial protein synthesis begins and elementary bodies convert into reticulate bodies.​

The reticulate cells replicate exponentially by binary fission.​

Upon cell stress, the reticulate bodies can enter a persistent state and transition into large aberrant bodies. They are then reactivated upon removal of this stress.​

During the late stage of infection, reticulate cells secrete late-cycle effectors and synthesise elementary body specific effectors before differentiating back into elementary bodies.​

Elementary bodies exit the host through lysis or extrusion (a pinching off of the host cells membrane containing many elementary bodies – survival advantage in extracellular environment).

47
Q

elementary bodies

A

non-replicating infectious particle found in the harsh extracellular environment. It contains a spore-like cell wall, composed of a network of proteins that are cross linked by disulfide bonds. This strong cell wall creates resistance to osmotic stress and physical stress.

48
Q

reticulate bodies

A

replicating, intracellular form of chlamydia spp. During differentiation of elementary bodies into reticulate bodies, the cell wall breaks down, increasing the fluidity of the cell for replication.​

​

49
Q

chlamydia in women

A

Pain when urinating ​

Dysuria​

Unusual vaginal discharge​

Abdominal/pelvic pain ​

Pain during sex​

Bleeding after sex or between periods​

Discharge from rectum ​

Eye redness, pain and discharge.

50
Q

chlamydia symptoms in men

A

Pain when urinating ​

Dysuria ​

White, cloudy or watery discharge from the tip of the penis ​

Burning or itching in the urethra ​

Pain in testicles ​

Discharge from rectum ​

Eye redness, pain and discharge

51
Q

gonorrhoea as a pathogen

A

Neisseria gonorrhoea – gram-negative, diplococcus, non-motile, anaerobic

52
Q

gonorrhoea symptoms female

A

an unusual vaginal discharge, which may be thin or watery and green or yellow in colour​

pain or a burning sensation when passing urine​

pain or tenderness in the lower abdominal area – this is less common​

bleeding between periods, heavy periods and bleeding after sex – this is less common

53
Q

gonorrhoea symptoms men

A

an unusual discharge from the tip of the penis, which may be white, yellow or green​

pain or a burning sensation when urinating​

inflammation (swelling) of the foreskin​

pain or tenderness in the testicles – this is rare

54
Q

herpes as a pathogen

A

Herpes simplex virus (HSV) - large, double-stranded DNA enclosed in a capsid, enveloped viruses

55
Q

herpes symptoms

A

spots or red bumps around the genital area​

pain inside the vagina, head of penis rectum​

vaginal discharge​

pain peeing or being unable to pee​

fever​

flu-like symptoms, backache, headache and a temperature​

mild swelling of the lymph glands in the groin, armpits and neck

56
Q

herpes recurrent symptoms

A

a tingling or burning sensation before blisters appear (this can signal the start of a recurrent infection)​

painful red blisters, which soon burst to leave ulcers​

pain inside the vagina, head of penis or rectum

57
Q

fact about herpes

A

once infected will remain in the body for life

58
Q

herpes transmission

A

kissing​

unprotected vaginal, anal or oral sex​

sharing sex toys that aren’t washed or covered with a new condom each time they’re used​

your genitals coming into contact with your partner’s genitals – this means you can get genital herpes from someone even if there is no penetration, orgasm or ejaculation

59
Q

oral herpes

A

HSV-1

60
Q

genital herpes

A

HSV-2

61
Q

genital warts pathogen

A

human papilloma virus
small, non-enveloped, icosahedral double-stranded DNA viruses.

62
Q

HPV transmission

A

any skin-to-skin contact of the genital area​

vaginal, anal or oral sex​

sharing sex toys

63
Q

what is a GUM clinic

A

genitourinary medicine

64
Q

most frequent presenting complaint at GUM

A

Urethral discharge, vaginal discharge, genital ulcers, lumps and bumps​

​

65
Q

services at GUM

A

testing and treatment for STIs​

advice and information about sexual health​

free condoms​

contraception​

pregnancy testing​

HIV testing and counselling ​

PEP and PrEP​

hepB vaccination​

abortion advice​

help for sexually assaulted victims​

referral to a specialist

66
Q

taking sexual history

A

Reason for attending/symptoms​

Sexual contacts (symptoms in contacts? number?)​

Sexual practices/ condom use​

Past history​

Recent AxB and allergies​

Medical/gynaecological history

67
Q

testing GUM clinics

A

Without vagina: First pass urine test, swabs from the urethra​

With vagina: Vaginal swab​

Homosexual men: Rectal/throat swabs​

Blood test: HIV and syphilis​

Physical genital examination

68
Q

gonorrhoea testing

A

Look for gram –ve intracellular diplococci

69
Q

chlamydia testing

A

PCR

70
Q

syphillis testing

A

Early or late. Starts asymptomatic

71
Q

genital herpes testing

A

HSV. Genital blisters. Not routinely testing but if you have a sore a sample will be taken from it.

72
Q

complications of untreated STI’s

A

Increase risk of HIV​

PID​

Orchitis​

Arthritis​

Encephalitis​

Neonatal infections​

Depression/anxiety​

Sexual dysfunction

73
Q

what must you do for a genital exam

A

Offer chaperone​

Obtain consent​

Keep discussion relevant​

Explain why its necessary​

Give privacy to un/dress​

Examine from mons pubic to natal cleft including the inguinal region​

For women: Speculum, lithotomy position, bimanual exam if required

74
Q

how to identify mycoplasma and trichmoniasis

A

swab

75
Q

purpose of liver palpation

A

check liver size
tenderness
masses

76
Q

technique to palpate liver

A

Patient in supine position, place your hand on patient’s right lower quadrant​

Ask patient to take a deep breath. Liver will move downwards due to downward movement of diaphragm, try to feel for liver edge as it descends ​

Palpate bottom margin of liver using fingers for texture i.e. soft, firm, hard, nodular.

77
Q

findings in liver palpation

A

Normal liver slightly tender; great tenderness suggests inflammation (e.g. hepatitis)/congestion (e.g. congestive heart disease)​

Normal liver is smooth with no irregularities; firm/bluntness/rounding/irregularity suggest abnormality. ​

Normal gallbladder not palpable; Obstructed, distended gallbladder may be palpable on inferior liver edge ​

Nodules may be palpable, rock hard, umbilicated suggesting malignancy

78
Q

method for liver ultrasound

A

Patient in supine position with their right hand above their head ​

Probe on right upper quadrant and slightly move it around the area

79
Q

what is a LFT

A

blood tests to help diagnose and monitor liver disease/ damage

80
Q

different LFT’s

A

alanine transaminase test, ALT
aspartate transaminase test, AST
alkaline phosphatase test, ALP
albumin test
bilirubin
gamma-glutamyltransferase, GGT
L-lactate dehydrogenase
coagulation

81
Q

alanine transaminase ALT

A

ALT enzyme found in liver breaks down proteins into energy for hepatocytes. When the liver is damaged, hepatocytes release ALT into the bloodstream + levels increase.​

High ALT indicates hepatitis, cirrhosis, cancer
normal= 3-40 iu/l

82
Q

aspartate transaminase test

A

AST enzyme metabolises amino acids. Normally present in blood at low levels. ​

High AST indicates liver damage, disease, muscle damage
normal= 3-30 iu/l

83
Q

alkaline phosphatase test

A

ALP enzyme found in liver + bone that breaks down proteins ​

High ALP indicates liver damage/disease e.g. blocked bile duct, bone disease
normal= 30-100 umol/l

84
Q

albumin test

A

Albumin is a protein made by liver responsible for modulating plasma oncotic pressure​

Low levels indicate liver damage/disease
normal= 35-50g/l

85
Q

bilirubin test

A

Bilirubin is a waste product of normal breakdown of red blood cells. Bilirubin passes through liver + excreted in stool​

High levels (jaundice) – liver damage or disease/anaemia
normal= 3-17 umol/l

86
Q

gamma glutamyltransferase GGT

A

GGT is enzyme found in blood, but mainly in liver. Acts as a catalyst to act certain body processes to occur. ​

High levels: liver, bile duct damage
normal= 8-60 u/l

87
Q

l-lactate dehydorgenase

A

LD is enzyme found in liver ​

High LD indicates liver damage

88
Q

coagulation test

A

Some clotting factors are produced by the liver ​

Prothrombin Time (PT) is time it takes blood to clot ​

High PT indicates liver damage, but can also be elevated if patient is on blood-thinning drugs e.g. warfarin.
PT= 10-14

89
Q

drug used

A

azithromycin

90
Q

alcohol hisotry

A

Quantity and frequency of alcohol consumed​

Patterns of use: regular drinking vs binge drinking ​

Duration of use: when they started drinking and for how long.​

Consequences and problems​

Family history ​

Alcohol-related symptoms​

Co-occurring conditions ​

Social support​

Treatment history​

Goals and motivation

91
Q

clinical tools used for alcohol use/dependency

A

AUDIT
AUDIT-C
FAST
CAGE

92
Q

AUDIT

A

Questionnaire to help in the self-assessment of alcohol consumption and risk for developing any alcohol-related problems.​

It consists of 10 questions on alcohol use.
Scoring system is used: higher score indicates a greater likelihood of problem. ​

Total score is calculated with feedback to the person.

93
Q

AUDIT-C

A

This assessment tool consists of the consumption questions from the AUDIT.
3 questions:
- how often do you have a drink containing alcohol
how many units of alcohol on typical day when drinking
how often have you had 6+ if female or 8+ if male in one single occasion in the last year

94
Q

FAST

A

shortened version of AUDIT, for use in busy A&E and hazard environments to detect hazardous drinking.

95
Q

CAGE

A

Quick test ​

C = cut down ​

A = annoyed ​

G = Guilty ​

E = eye-opener

96
Q

support mechanisms for someone struggling with alcohol

A

AA (Alcoholics Anonymous): individuals can share their experiences, receive guidance and obtain support.​

Counselling and therapy: Explore their relationship with alcohol and develop strategies to manage alcohol use.​

Online resources and mobile apps: self-help tools, such as tracking alcohol use and setting goals.​

Helplines and hotlines: provide individuals with confidential and immediate means of seeking support.

97
Q

health inequalities definition

A

Health inequalities are usually defined as systematic differences in health outcomes between socioeconomic groups, categorized by indicators such as household income, educational qualifications and area deprivation.

98
Q

alcohol harm paradox

A

Affordability is a key driver of consumption.​

Health harms are much more pronounced in areas of high deprivation, despite average consumption usually being lower in these areas.​
“

Deprivation weakens the protective factors and strengthens the risk factors.

99
Q

effect of alcohol on children

A

Children can be greatly affected by alcoholism in their household.​

They can become frustrated and angry, as they try to make sense of why the person that they care about is behaving in such as way.​

Alcoholism can make parents impulsive and unstable.​

Older children of alcoholics can suffer from obsessive perfectionism, hoarding, isolation and excessive self-consciousness.​

They can have difficulty at school.​

These emotions and thoughts that present themselves in childhood can be carried into adulthood.

100
Q

effect of alcohol on spouses, partners and family members

A

Whilst the person with alcohol addiction experiences the brunt of the physical problems, the people who are closes to them often share the emotional side effects of the person’s addiction.​

Alcohol abuse has the potential to destroy families.​

Family members may become the victims of physical or emotional outbursts.​

Relationships are built on trust, but many alcoholics lie or blame others for their problems. They are often in denial.​

It can on a family’s finances due to how expensive it is.

101
Q

coping with addiciton

A

Accepting addiction​

Breaking patterns​

Self-esteem and self-worth​

Managing emotions​

Seeking support

102
Q

barriers to treatment

A

Lack of knowledge​

Social Stigma​

Fear of confidentiality breaches​

Limited access to healthcare services ​

Cultural and religious beliefs

103
Q

sexual health stigmas

A

STD/STI stigma​

HIV/AIDS​

Contraception​

Abortion​

Sexual dysfunction​

LGBTQ+​

Sex work stigma ​

Mental health stigma

104
Q

HIV stigma

A

HIV/AIDS Stigma: HIV/AIDS-related stigma is a particularly pervasive and longstanding issue. People living with HIV/AIDS often encounter prejudice, fear, and discrimination due to misconceptions about transmission routes, moral judgments, and associated stereotypes.

105
Q

std stigma

A

STD/STI Stigma: People diagnosed with sexually transmitted infections (STIs) may face significant stigma and discrimination. There can be a misconception that STIs are solely associated with promiscuity or irresponsible behavior, leading to judgment, blame, and social exclusion.

106
Q

contraception stigma

A

Contraception Stigma: Discussions around contraception can be met with judgment and moralizing attitudes. Some individuals may perceive the use of contraception as a sign of promiscuity or an invitation for sexual activity, leading to stigmatization.

107
Q

abortion stigma

A

Abortion Stigma: Abortion remains a highly stigmatized topic in many societies. Individuals who have undergone abortions may face condemnation, shame, and social ostracism due to moral, religious, or cultural beliefs.

108
Q

sexual dysfunction stigma

A

Sexual Dysfunction Stigma: Individuals experiencing sexual dysfunctions, such as erectile dysfunction or low libido, can face stigma due to societal expectations surrounding sexual performance and desirability. This can lead to feelings of embarrassment, shame, and a reluctance to seek help.

109
Q

LQBTQ+ stimga

A

LGBTQ+ Stigma: Sexual health stigmas also affect LGBTQ+ individuals. Homophobia, biphobia, and transphobia can lead to marginalization, discrimination, and barriers to accessing appropriate sexual healthcare.

110
Q

sex work stigma

A

: Stigma towards individuals involved in sex work is pervasive and often results in social, legal, and economic marginalization. Sex workers face discrimination, violence, and limited access to healthcare services.

111
Q

mental health stigma

A

The intersection of sexual health and mental health can also be stigmatized. People with mental health conditions related to sexuality, such as sexual addiction or gender dysphoria, may face judgment and misunderstanding.

112
Q

effects of stigma on an indivduals mental health

A

They may discourage individuals from seeking healthcare, support, or information, leading to delayed or inadequate treatment leading to a worse condition associated with sexual health issues.

113
Q

what could be done about stigma around sexual health

A

Education and awareness​

Normalising discussions​

Confidentiality and privacy ​

Accessible and affordable services​

Engaging communities and religious leaders​

Peer support and counseling ​

Targeted campaigns

Medicine: PBL wrap-ups (21 decks)

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