Module 15 Flashcards
1
Q
Warts/Verrucae
A
- Benign lesions of the skin caused by HPV
- Round and elevated with rough, grayish surface
- Common Warts (Verrucea vulgaris)
- Around fingernails – periungual warts
- Plantar Warts (Verrucae plantaris)
- Found in warm moist environments
- Found at pressure points
- Filiform Warts
- Long and narrow
- Eyelids, face, neck
- Genital Warts
- Condyloma acuminata vs.
- Condyloma lata - ?
- Second stage of syphilis
- Examination under darkfield microscopy will show spirochetes
- Warts are spread by person/object to person contact
- Common Warts (Verrucea vulgaris)
2
Q
Abscesses
A
- Collection of pus (dead white blood cells and bacteria with tissue debris and serum), surrounded by inflammation
- Causes
- Infection
- Around hair follicle- folliculitis
- Furuncle > S. aureus - Also: hot tubs (Pseudomonas)
- Carbuncle> collection of infected hair follicles
- Tooth infection > periapical abscess
- Intestinal > ruptured appendix, perforated bowel
- Retropharyngeal > spread of infection from tonsils, teeth, sinuses, ear
- Muffled voice, drooling, stiff neck, very painful, stridor
- Signs and Symptoms
- Painful, red, warm area
with pus/infectious material - If not treated > sepsis
- Painful, red, warm area
- Testing
- Clinical
- CBC
- Wound culture
- CT
3
Q
Periapical Abscess
A
Infection of pulp
4
Q
Intussusceptions/Volvulus
A
- Causes
- Intussusception: Telescoping of one part of the intestine into another
- Idiopathic, Viral infection
- Bowel obstruction and cut-off blood supply
- Vomitting, abdominal pain, red currant jelly stools
- Intestinal obstructions in infants: untreated=death
- 60-70% success on enema under fluoroscopic guidance (surgery if unsuccessful)
- Volvulus: Twisting of intestines
- Malrotation in development
- Intestinal obstruction and cut-off blood supply
- Acute and severe
- Bilious vomiting (77-100%), abdominal pain colic
- Immediate surgery
- Intussusception: Telescoping of one part of the intestine into another
- Testing
- Clinical
- X-Ray, CT, US
5
Q
Volvulus
A
Massive sigmoid volvulus. Barium enema of the colon shows a tapered obstruction at the rectosigmoid junction with a typical bird’s-beak deformity (black arrow).
6
Q
Hirschsprung’s Disease– Congenital Megacolon
A
- Causes
- Missing intestinal/rectal ganglion cells
- Malformation of the Parasympathetic NS (80% rectal end)
- Inherited?
- Main cause of colon obstruction (infants)
- Missing intestinal/rectal ganglion cells
- Signs and Symptoms
- Delayed meconium stool at birth
- Vomiting, colic, distended abdomen (gives the name megacolon), “ribbon-like stool”
- Toxic- enterocolitis > life threatening, fever, swollen abdomen, explosive and bloody diarrhea
- Testing
- Anorectal manometry
- tests sphincter muscle strength and nerve supply
- CT/X-Ray
- Rectal Biopsy
- Anorectal manometry
- Ganglia in parasympathetic are located far away from the spinal cord
- Sympathetic and parasympathetic is a two neuron system to get to the target neuron
- In this case the target organ is the colon
- They don’t have ganglia cells in congenital megacolon
- They are missing ability to produce para something waves
- If fecal material can’t move it builds up so the colon enlarges proximal, before, the area that is missing the ganglia
- Toxic entercolitis is bad it is a build-up of fecal matter in the colon
anorectal manometry they put a ballon into rectal area - When rectum stretches due to fecal matter the spincter SHOULD relax
7
Q
Hirschsprung’s Disease– Congenital Megacolon
A
Dilation of bowel (megacolon) proximal to the affected region of narrowing at the lower left center in sigmoid colon. Mucosal damage and secondary infection may follow.
8
Q
Hirschsprung’s Disease– Congenital Megacolon
A
A barium enema showing a “long segment” Hirschsprung’s disease. The transition zone is in the large intestine in an area going across the abdomen called the transverse colon. The arrow demonstrates the area of the transition zone between the enlarged area which has ganglion cells (normal) and the small area which does not (Hirschsprung’s disease).
- When patient swallows Barium you will be able to see the dilated bowel
Everything proximal to it is full, it can’t move
Side note: review autonomic nervous system: parasympathetic and sympathetic
9
Q
Meckel’s Diverticulum
A
- Outpouching of small intestine in kids
- 1.5 – 2 feet from ileocecal valve
- Causes
- Idiopathic - developmental
- Signs and Symptoms
- Asymptomatic
- Painless rectal bleeding
- Diverticulitis
- Testing
- Frequently suspected, seldom found
- US/CT
- Radionucleotide scintingraphy (Meckel Scan)
- Small outpouching
- Can do a scan to look for the outpouching
10
Q
Meckel’s Diverticulum
A
Meckel’s Diverticulum scintigraphy performed on 2 year old boy with intermittent bleeding (bright red blood) and no other accompanying symptom. Sequential images obtained after injection of99mTc-pertechnetate show obvious accumulation of radioactivity in right lower paraumbilical region, consistent with most frequent location of Meckel’s diverticulum.
- Can inject patient in order to look for disease
11
Q
Polycystic Ovarian Syndrome (PCOS)
A
- 1 out of 15 women: main cause of hormonal disease of women at childbearing age
- Causes
- Genetic
- Unknown: Hormonal imbalance
- Increased insulin (due to resistance) causes increase in androgen (male sex hormone) production?
- Signs and Symptoms
- Ovaries with multiple cysts
- increase LH secretion > increase Androgens (T, androstenedione, DHEA) > increase conversion to Estrogen without enough Progesterone to balance > endometrial hyperplasia > risk endometrial CA
Irregular or absent menses (due to high estrogen exerting negative feedback on FSH)
– Infertility Virilization – females gain male traits (inc body hair distribution) - Obesity (41% are obeses)
- Insulin resistant (prediabetes or DM type 2) (can lead to type 2 diabetes)
- Acanthosis nigricans – a result of having insulin resistance (this is the photo, the darkening of the skin)
- Higher incidence of
- HTN
- Hyperlipidemia
- Nonalcoholic Steatohepatitis (NASH)
- Fatty liver
- Elevated CRP > CV risks
- Testing
- Hormones
- US/CT
- R/O sources of hormone secretion
- TX: No cure, treat the symptoms
- Very common
- Differs from one female to another
- Hormonal imbalances is a huge cause
- There is a correlation but not a causation with increased insulin
- The male sex hormones are converted to estrogen which is a normal process.
- The longer a women is exposed to estrogen the higher the risk for developing endometrial cancer.
12
Q
Polycystic Ovarian Syndrome (PCOS)
A
- LH is abnormally high and stays high this goes to theca cells in the ovary which make androgens (male sex hormones) this can lead to hirsutism (excess hair)
- Normally excess androgens should loop back and do a negative feedback but with this disease it stays high and FSH is low. Normally FSH tells the granulosa to mature but with this disease there is no egg release. (that is why it can lead to infertility)
13
Q
Diabetes Mellitus
A
- Abnormal Blood Glucose metabolism
- Causes
- Pre- DM > ?
- Increased Waist to Hip Ratio, Stage 1 HTN, Hyperlipidemia, Acanthosis Nigricans
- PCOS
- Will develop Type 2 within 10 years unless lose 5-7% of body weight
- Type 1 (IDDM) > Autoimmune attacks beta cells
- Juvenile and IDDM – peaks at age 12 for onset
- DKA - (Metabolic acidosis) – “Fruity” breath
- Lose weight due to burning proteins/fats for fuel
- Type 2 (NIDDM) > Lifestyle, medications
- Decreased insulin production
- Insulin resistance
- Gestational DM > Pregnancy
14
Q
Diabetes Mellitus Type 2
A
- 90-95% of Diabetes in the U.S.
- 60-80% are obese
- Life expectancy decreases 5-10% for middle aged populations
- 3 Pathological changes
- 1) Insulin production decreases
- Beta cells are destroyed – Islet cell burnout
- Amyloid formation in pancreas -10-40%
- Lipid accumulation
- Sensitive to high levels of glucose and free fatty acids
> Apoptosis - Cytokines from adipose tissue
2) Insulin resistance
- Decrease of insulin receptors on cells
- Initially body is able to ‘keep up’ by producing more insulin
3) Excessive glucose production (gluconeogenesis) and breakdown of glycogen (glycogenolysis) by the liver – alpha cells become less responsive to the negative feedback inhibition of glucose produce more glucagon.
- Initially body is able to ‘keep up’ by producing more insulin
- Beta cells are destroyed – Islet cell burnout
15
Q
Diabetes Mellitus
s/s
testing
A
- Signs and Symptoms
- 3 P’s: Polyuria, Polydipsia, Polyphagia
- Neuropathies > retinopathy, nephropathy, peripheral neuropathy
- Increased infections (UTI, yeast), gingivitis, dry skin, blurred vision
- Aconthosis nigricans, skin tags, obesity, skin changes
- PCOS
- Testing (DM)
- Fasting glucose > 126mg/dL
- Hemoglobin A1c: Glycated hemoglobin - Sugar sticks to Hb (patient can’t cheat on checkups!) (Can check for the past few months so they can’t cheat)
- Normal: Less than 5.7%
- Pre-diabetes: Between 5.7% - 6.4%
- Diabetes: 6.5% or higher
- Testing: you want the fasting glucose level to be under 100
Hb will grab onto sugar
A person’s blood sugar can change in hours, to minutes, to days
16
Q
Acanthosis Nigricans
A
Diabetes Mellitus
17
Q
Diabetes Mellitus Type 2 Tx
A
- A lot of classes of medication
- If all of these fail you have to give an injection of insulin therapy
- If someone is pre-diabetic they need to eat healthy and cut back their sugar. Tell patient to cut out sugar, carbohydrates, you need to educate your patients
18
Q
Renal Failure
A
- Loss of kidney function
- Causes
- Prerenal
- Renal
- Postrenal
- Signs and Symptoms
- Decreased U/O, Edema, Dyspnea, Fatigue, Confusion, Seizures
- Testing
- Daily U/O
19
Q
Renal Failure
A
- Intrinsic means within
- Study this (slide 40)
- Bacterial sepsis can cause a drop in blood pressure
- Stenosis is narror. (renal artery stenosis is narrowing)
- Postrenal major cause is what? EXAM
- Study each of these
- Acute glomerulonephritis is a problem with the filter
- Acute interstitial nephritis is a problem with the tissue surrounding renal tubule
20
Q
Glomerulonephritis
A
- Decreased ability of the kidneys to filter
- Causes
- SLE, Autoimmune, Post-strep glomerulonephritis, Bacterial Endocarditis
- HTN, DM
- *Berger’s disease (don’t confuse with burgers disease, thromboangitis obliyerans)
- Signs and Symptoms
- Proteinurea, hematuria (cola colored urine), HTN, edema, decreased urinary output
- Testing
- BUN, Creatinine, CT, Biopsy
- There are a bunch of autoimmune disorders that could cause glomerulonephritis
- Normally proteins are way too big to be filtered out
- What holds water in the blood vessels? Albumin which is a protein
- The right kidney is lower than the left because of the liver
21
Q
IgA NEPHROPATHY - BERGER’S DISEASE
A
- IgA deposition in glomeruli
- Causes
- FHX, widespread Vasculitis
- Signs and Symptoms
- Progresses slowly over years
- Young men
- Dark brown/bloody/rust color urine
- Can lead to renal failure
- Testing
- Proteinurea, hematuria- cola colored urine, HTN, edema, decreased urinary output
- UA, Biopsy for the definitive Dx (IgA deposits)
- Treatment
- No cure, but meds can slow progress
- Antibodies clogging up the glomerular capillaries in the kidneys.
22
Q
ATN
A
- Death of tubular epithelial cells that form the renal tubules of the kidneys - one of the most common causes of AKI (Acute Kidney Injury)
- Causes
- Ischemia - renal artery stenosis, shock. embolism of the renal arteries
- Nephrotoxic drugs - antibiotics such as aminoglycosides (class of antibiotics), statins such as atorvastatin, and cytoxic drugs such as cisplatin, or by intoxication (ethylene glycol, “anti-freeze”). (have to watch someone’s kidney function)
- Signs and symptoms
- The presence of “muddy brown casts” of epithelial cells found in the urine during urinalysis is pathognomonic for ATN.
- Tx
- Aggressive treatment of the factors that precipitated ATN (e.g. hydration and stop of the offending drug).
- Prognosis
- Because the tubular cells continually replace themselves, the overall prognosis for ATN is quite good if the cause is corrected, and recovery is likely within 7 to 21 days
- A lot of things can cause ATN
- Usually not irreversible
- Renal tubular cells can regenerate and heal
- Nephrotoxic drugs the list is huge
- High anion gap
- ATN is acute tubular necrosis
- Muddy brown casts is a good marker for ATN
23
Q
Nephrotic Syndrome
A
- Nonspecific kidney disorder characterized by a number of signs of disease:
- Proteinuria, hypoalbuminemia and edema
- Increase in permeability of the capillary walls of the glomerulus high levels of protein passing from the blood into the urine low levels of protein in the blood (hypoproteinemia or hypoalbuminemia), ascites, edema, high cholesterol, and a predisposition for coagulation
- Spaces between podocytes, enlarges enough to permit proteinuria (and subsequently hypoalbuminemia), but not large enough to allow cells through (hence no hematuria).
- By contrast, in nephritic syndrome red blood cells pass through the pores, causing hematuria
- Generically there is protein in the urine and there is not enough albumin
- General patho is they loose protein so they lose the ability to hold water in the blood
- If blood cells are passing through into the urine= nephritic syndrome
24
Q
Nephrotic Syndrome
A
Features of Nephrotic syndrome- NAPHROTIC
- Na+ decrease (hyponatremia)
- Albumin decrease (hypoalbuminemia)
- Proteinuria >3.5 g/day
- Hyperlipidemia
- Renal vein thrombosis
- Orbital edema
- Thromboembolism
- Infection (due to loss of immunoglobulins in urine)
- Coagulability (due to loss of Antithrombin III in urine)
- Orbital edema is puffiness around the eyes
- Immunoglobulins are IgG, IgA, IgD, IgM, IgE, if you lose these you lose your defense mechanisms against pathogens
- Normally antithrombin III deactivates thrombin
25
Nephrotic Syndrome
- Signs and Symptoms
* Hypoalbuminemia (Why?)
* Hyperlipidaemia
* Edema (which is generalized and also known as anasarca or dropsy) that begins in the face
* Lipiduria (lipids in urine) can also occur, but is not essential for the diagnosis of nephrotic syndrome
* Hyponatremia (Why?)
- Explanations of S/Sx:
* The most common sign is excess fluid in the body due to the serum hypoalbuminemia. Lower serum oncotic pressure causes fluid to accumulate in the interstitial tissues. Sodium and water retention aggravates the edema. This may take several forms:
- Puffiness around the eyes, characteristically in the morning
- Pitting edema over the legs
- Fluid in the pleural cavity causing pleural effusion. More commonly associated with excess fluid is pulmonary edema
- Fluid in the peritoneal cavity causing ascites
* Anemia (iron resistant microcytic hypochromic type) may be present due to transferrin loss
* Dyspnea may be present due to pleural effusion or due to diaphragmatic compression with ascites
* Some patients may notice foamy or frothy urine, due to a lowering of the surface tension by the severe proteinuria
* As a response to hypoproteinemia the liver commences a compensatory mechanism involving the synthesis of proteins, such as lipoproteins causes the hyperlipidemia
26
Nephrotic Syndrome
- Primary nephrotic syndrome - glomerular disease that is limited to the kidney, (primary glomerulonephritis)
- Secondary nephrotic syndrome - a condition that affects the kidney and other parts of the body
- PRIMARY CAUSES of nephrotic syndrome (Thesre are considered to be "diagnoses of exclusion", i.e. they are diagnosed only after secondary causes have been excluded)
* Minimal change disease (MCD): is the most common cause of nephrotic syndrome in children. It owes its name to the fact that the nephrons appear normal when viewed with an optical microscope as the lesions are only visible using an electron microscope. Another symptom is a pronounced proteinuria.
* Focal segmental glomerulosclerosis (FSGS): is the most common cause of nephrotic syndrome in adults. It is characterized by the appearance of tissue scarring in the glomeruli. The term focal is used as some of the glomeruli have scars, while others appear intact; the term segmental refers to the fact that only part of the glomerulus suffers the damage.
* Membranous glomerulonephritis (IMN): The inflammation of the glomerular membrane causes increased leaking in the kidney. It is not clear why this condition develops in most people, although an auto-immune mechanism is suspected.
* Mesangial proliferative glomerulonephritis (MPGN): is the inflammation of the glomeruli along with the deposit of antibodies in their membranes, which makes filtration difficult.
* Rapidly progressive glomerulonephritis (RPGN): (Usually presents as a nephritic syndrome) A patient’s glomeruli are present in a crescent moon shape. It is characterized clinically by a rapid decrease in the glomerular filtration rate (GFR) by at least 50% over a short period, usually from a few days to 3 months.
-General
Do not have to know them now
27
Nephrotic Syndrome
- SECONDARY CAUSES of nephrotic syndrome:
* Diabetic nephropathy: is a complication that occurs in some diabetics. Excess blood sugar accumulates in the kidney causing them to become inflamed and unable to carry out their normal function. This leads to the leakage of proteins into the urine.
* Systemic lupus erythematosus: this autoimmune disease can affect a number of organs, among them the kidney, due to the deposit of immunocomplexes that are typical to this disease. The disease can also cause lupus nephritis.
* Sarcoidosis: This disease does not usually affect the kidney but, on occasions, the accumulation of inflammatory granulomas (collection of immune cells) in the glomeruli can lead to nephrotic syndrome.
* Syphilis: kidney damage can occur during the secondary stage of this disease (between 2 and 8 weeks from onset).
* Hepatitis B: certain antigens present during hepatitis can accumulate in the kidneys and damage them.
* Sjögren's syndrome: this autoimmune disease causes the deposit of immunocomplexes in the glomeruli, causing them to become inflamed, this is the same mechanism as occurs in systemic lupus erythematosus.
* HIV: the virus’ antigens provoke an obstruction in the glomerular capillary’s lumen that alters normal kidney function.
* Amyloidosis: the deposit of amyloid substances (proteins with anomalous structures) in the glomeruli modifying their shape and function.
* Multiple myeloma: the cancerous cells arrive at the kidney causing glomerulonephritis as a complication.
* Vasculitis: inflammation of the blood vessels at a glomerular level impedes the normal blood flow and damages the kidney.
* Cancer: as happens in myeloma, the invasion of the glomeruli by cancerous cells disturbs their normal functioning.
* Genetic disorders: congenital nephrotic syndrome is a rare genetic disorder in which the protein nephrin, a component of the glomerular filtration barrier, is altered.
* Drugs ( e.g. gold salts, penicillin, captopril): gold salts can cause a more or less important loss of proteins in urine as a consequence of metal accumulation. Penicillin is nephrotoxic in patients with kidney failure and captopril can aggravate proteinuria.
28
Nephrotic Syndrome
- Restrict salt intake (Why?)
- Tx of kidney damage
* Corticosteroids: decreases the proteinuria and the risk of infection as well as a resolution of the edema.
* Immunosupressants (cyclophosphamide): only indicated in recurring nephrotic syndrome in corticosteroid dependent or intolerant patients. A possible side effect of the cyclophosphamide is alopecia. Complete blood count tests are carried out during the treatment in order to give advance warning of a possible infection
-Restrict their salt intake because you want to get rid of excess fluid
Don’t need to know all of the immunosupressants
29
Wilm's Tumor (rare) 1 in 10,000 children
- Mixed tumor of the kidney in children
- Causes
* Unknown
* Chromosome #11
- Mutation
- Inherited
- S/S
*
30
Lung cancer
- Leading cause of death in US
- Smoking (85%)
- Small cell carcinoma/ Oat cell carcinoma (CA cells are small)
* Smokers
* SIADH (too much ADH), ectopic ACTH (paraneoplastic syndromes resulting from tumor-produced substances)
- Non-small cell carcinoma
* Smoking, Second-hand smoke exposure, metastasis, toxins (asbestos)
- Adeonocarcinoma
- Signs and Symptoms
* Dyspnea, SOB, hemoptysis, persistent cough or changes in chronic/smokers cough
