Unit 8 Week 2: Chlamydia and risky behaviour Flashcards
physiological functions of the liver
bile production
carbohydrate metabolism
lipid metabolism
protein and ammonia metabolism
storage functions
bile production liver
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
components of carbohydrate metabolism
glycogenolysis
gluconeogenesis
glycolysis
glycogenesis
glycogenolysis
liver can break down glycogen, stored form of glucose, into glucose-6-phosphate. This process is stimulated by the hormone glucagon
gluconeogenesis
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
glycolysis
liver can also use glucose for energy, glucose is converted into pyruvate, enters citric acid cycle to generate ATP
glycogenesis
can store excess glucose as glycogen. Stimulated by the hormone insulin
componetns of lipid metabolism
lipogenesis
lipolysis
beta oxidation
lipoprotein metabolism
lipogenesis
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
lipolysis
breaking down and storing fat into fatty acids. Stimulated by hormones such as glucagon and adrenaline
beta oxidation
beta oxidation of fatty acids into acetyl-CoA, which then enters the citric acid to generate ATP
lipoprotein metabolism
involved in the synthesis and metabolism of lipoproteins which are responsible for transporting lipids through the body, low and high density lipoproteins
components of protein and ammonia metabolism
protein synthesis
amino acid catabolism urea cycle
protein synthesis
synthesis many plasma proteins, including albumin, fibrinogen and globulins, these proteins are responsible for maintaining osmotic pressure and transporting molecules
amino acid catabolism
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
urea cycle
converting toxic ammonia into urea, involves a series of enzymatic reactions that occur in the liver, resulting urea is excreted in the urine
storage functions of the liver
glycogen
vitamins
minerals
drug and toxin
glycogen storage
liver stores glycogen, broken down into glucose when the body needs energy
vitamin storage
storage of several vitamins, including vitamins A, D and b12, released into blood stream when needed
mineral storage
stores minerals such as Iron and copper, these are used for a variety of functions such as oxygen transport and enzyme function
drug and toxin storage
can store certain drugs and toxins, can accumulate in the liver overtime, can lead to liver damage or dysfunctions if it reaches toxic levels
pathophysiology of alcohol related liver disease
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
alcohol metabolism via ADH pathways
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.
alcohol metaoblism via MEOS pathway
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.
hepatic fat accumulation
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.
endotoxins in the gut due to alcohol
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
oxidative stress increases
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
resultant inflammation cell death and fibrosis as result of alcohol
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
cause of alcoholic fatty liver, steatosis
lipid accumulation:
FA uptake increases
lipogenesis increases
beta oxidation decreases
VLDL release decreases
cause of alcohol steatoheptatitis
inflammation:
kupffer cell activation
TLR4/NFKb pathway
cytokine/ ROS increases
cause of alcohol fibrosis/ cirrhosis
fibrosis:
protein adduct
PKC and TGF beta pathway
profibrotic effect of ROS
cause of heptatocellular carcinoma
carginogenesis:
DNA/protein adduct
dna integrity decreases
dna repair decreases
3 stages of alcohol related liver disease
alcoholic fatty liver disease
alcoholic heptatitis
cirrhosis
alcoholic fatty liver disease
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.
alcoholic hepatitis
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.
liver cirrhosis
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.
treatment for alcohol related liver disease
no specific medical treatment
stop drinking
liver transplant may be required
effects of alcohol on gall bladder
Small amounts = reduce risk of gallstones and gallbladder pain
Heavy drinking = lead to gallbladder problems and pain
effects of alcohol on the brain physically
Difficulty walking
Blurred vision
Slurred speech
Slowed reaction times
Impaired memory
Alcohol-related brain damage (ARBD), e.g Wernicke–Korsakoff syndrome
effect of alcohol on the brain psycholocially
depressant
affects inihibtion
depression
slows cognitive functioning
how cna dependency develop
long temr alcohol uses and reduces number of neurotransmitters in our brains
need some to ward off anxiety and depression so drink to relieve
alcohol damage to nerve cells
toxic
can cause brain cells to die
brain tissue shrink
damage to blood vessle alcohol
can lead to high blood pressure
alcohol and mental health
depression
anxiety
psychosis
suicide and self harm
chlamydia as a pathogen
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.
pathophysiology of chlamydia
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).
elementary bodies
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.
reticulate bodies
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.
chlamydia in women
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.
chlamydia symptoms in men
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
gonorrhoea as a pathogen
Neisseria gonorrhoea – gram-negative, diplococcus, non-motile, anaerobic
gonorrhoea symptoms female
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
gonorrhoea symptoms men
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
herpes as a pathogen
Herpes simplex virus (HSV) - large, double-stranded DNA enclosed in a capsid, enveloped viruses
herpes symptoms
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
herpes recurrent symptoms
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
fact about herpes
once infected will remain in the body for life
herpes transmission
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
oral herpes
HSV-1
genital herpes
HSV-2
genital warts pathogen
human papilloma virus
small, non-enveloped, icosahedral double-stranded DNA viruses.
HPV transmission
any skin-to-skin contact of the genital area
vaginal, anal or oral sex
sharing sex toys
what is a GUM clinic
genitourinary medicine
most frequent presenting complaint at GUM
Urethral discharge, vaginal discharge, genital ulcers, lumps and bumps
services at GUM
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
taking sexual history
Reason for attending/symptoms
Sexual contacts (symptoms in contacts? number?)
Sexual practices/ condom use
Past history
Recent AxB and allergies
Medical/gynaecological history
testing GUM clinics
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
gonorrhoea testing
Look for gram –ve intracellular diplococci
chlamydia testing
PCR
syphillis testing
Early or late. Starts asymptomatic
genital herpes testing
HSV. Genital blisters. Not routinely testing but if you have a sore a sample will be taken from it.
complications of untreated STI’s
Increase risk of HIV
PID
Orchitis
Arthritis
Encephalitis
Neonatal infections
Depression/anxiety
Sexual dysfunction
what must you do for a genital exam
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
how to identify mycoplasma and trichmoniasis
swab
purpose of liver palpation
check liver size
tenderness
masses
technique to palpate liver
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.
findings in liver palpation
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
method for liver ultrasound
Patient in supine position with their right hand above their head
Probe on right upper quadrant and slightly move it around the area
what is a LFT
blood tests to help diagnose and monitor liver disease/ damage
different LFT’s
alanine transaminase test, ALT
aspartate transaminase test, AST
alkaline phosphatase test, ALP
albumin test
bilirubin
gamma-glutamyltransferase, GGT
L-lactate dehydrogenase
coagulation
alanine transaminase ALT
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
aspartate transaminase test
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
alkaline phosphatase test
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
albumin test
Albumin is a protein made by liver responsible for modulating plasma oncotic pressure
Low levels indicate liver damage/disease
normal= 35-50g/l
bilirubin test
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
gamma glutamyltransferase GGT
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
l-lactate dehydorgenase
LD is enzyme found in liver
High LD indicates liver damage
coagulation test
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
drug used
azithromycin
alcohol hisotry
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
clinical tools used for alcohol use/dependency
AUDIT
AUDIT-C
FAST
CAGE
AUDIT
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.
AUDIT-C
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
FAST
shortened version of AUDIT, for use in busy A&E and hazard environments to detect hazardous drinking.
CAGE
Quick test
C = cut down
A = annoyed
G = Guilty
E = eye-opener
support mechanisms for someone struggling with alcohol
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.
health inequalities definition
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.
alcohol harm paradox
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.
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Deprivation weakens the protective factors and strengthens the risk factors.
effect of alcohol on children
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.
effect of alcohol on spouses, partners and family members
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.
coping with addiciton
Accepting addiction
Breaking patterns
Self-esteem and self-worth
Managing emotions
Seeking support
barriers to treatment
Lack of knowledge
Social Stigma
Fear of confidentiality breaches
Limited access to healthcare services
Cultural and religious beliefs
sexual health stigmas
STD/STI stigma
HIV/AIDS
Contraception
Abortion
Sexual dysfunction
LGBTQ+
Sex work stigma
Mental health stigma
HIV stigma
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.
std stigma
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.
contraception stigma
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.
abortion stigma
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.
sexual dysfunction stigma
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.
LQBTQ+ stimga
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.
sex work stigma
: 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.
mental health stigma
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.
effects of stigma on an indivduals mental health
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.
what could be done about stigma around sexual health
Education and awareness
Normalising discussions
Confidentiality and privacy
Accessible and affordable services
Engaging communities and religious leaders
Peer support and counseling
Targeted campaigns
